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Gastrointestinal > Liver and Biliary Tree Pathology > Flashcards

Liver and Biliary Tree Pathology Flashcards

1
Q

What is the broad functions of the liver?

A
  1. Storage.
  2. Synthesis.
  3. Metabolism/detoxification.
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2
Q

What does the liver store?

A
  1. Glycogen.
  2. Vitamins.
  3. Iron.
  4. Copper.
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3
Q

What does the liver synthesise?

A
  1. Glucose.
  2. Protein.
  3. Lipid and cholesterol.
  4. Bile.
  5. Coagulation Factors.
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4
Q

What does the liver metabolise?

A
  1. Bilirubin.
  2. Ammonia.
  3. Carbohydrates and lipids.
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5
Q

What does the liver detoxify?

A
  1. Drugs.

2. Alcohol.

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6
Q

What is cirrhosis?

A

Irreversible state of inflammation of the liver, in response to any chronic liver injury.

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7
Q

What are the characteristics of cirrhosis.

A
  1. Ongoing inflammation causes fibrosis.
  2. Association with hepatocyte necrosis.
  3. Resulting architectural changes of nodules.
    Changes occur over years.
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8
Q

What is the end result of cirrhosis?

A
  1. Impairment of liver function.

2. Distortion of architecture leads to vascular changes (portal hypertension).

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9
Q

Describe Alcoholic Liver Disease.

A

Can occur after exposure of alcohol. There are 3 stages, the final one is cirrhosis. It is associated with a build up of acetaldehyde (a product of alcohol metabolism).

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10
Q

What are the stages of Alcoholic Liver Disease?

A
  1. Fatty change: occurring over weeks, which is initially reversible.
  2. Alcoholic Hepatitis: occurring over years and is initially reversible.
  3. Cirrhosis: occurring over years, it is an end stage and is irreversible damage.
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11
Q

How do the stages of Alcoholic Liver Disease present histologically?

A

In a fatty liver white spaces of fat appear.
In alcoholic hepatitis there is fibrosis in the fatty liver, shown as blue bands.
In cirrhosis there is fibrosis surrounding healthy liver tissue.
Cirrhosis can lead to hepatocellular carcinoma.

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12
Q

How can Alcoholic Liver Disease be identified?

A

Through the patients history.

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13
Q

How might someone with Alcoholic Liver Disease present?

A

The patient may be asymptomatic or have general symptoms of liver disease.
In fatty liver the patient may have hepatomegaly (enlarged liver).
In alcoholic hepatitis there may be rapid onset of jaundice, tender hepatomegaly (RUQ pain) or symptoms of a more severe disease (nausea, oedema and ascites, splenomegaly).

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14
Q

How do you manage Alcoholic Liver Disease?

A

Try and reduce alcohol intake before cirrhosis occurs. Do this in a controlled way.

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15
Q

Describe characteristics of Viral Hepatitis.

A

Caused by chronic Hepatitis B or C which are blood borne viruses with the potential for chronic infection. This causes an increased risk for hepatocellular carcinoma.

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16
Q

Describe the clinical characteristics of Hepatitis B.

A

Has a vaccine.
Has no cure.
May have symptoms of acute infection.

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17
Q

Describe the clinical characteristics of Hepatitis C.

A

Has a cure.
No vaccine.
Most are asymptomatic during acute inflammation.

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18
Q

Describe the Pathogenesis of Non-Alcoholic Fatty Liver Disease (NAFLD).

A

Similar pathogenesis to ALD but without the alcohol. Associated with an accumulation of triglycerides and other lipids in hepatocytes.

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19
Q

What are the risk factors of NAFLD?

A
  1. Obesity.
  2. Diabetes.
  3. Metabolic syndrome (dyslipidaemia).
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20
Q

How do you manage NAFLD?

A

Reduce the risk factors by lifestyle modification.

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21
Q

How can Hereditary Haemochromatosis cause Cirrhosis?

A

There is abnormal iron metabolism so there is increased absorption of irons from the small intestine so excess deposition. This can affect the liver and other organs. There is elevated iron and ferritin levels. If the liver is affected there will be abnormal LFTs.

22
Q

What is the genetic characteristic of Hereditary. Haemochromatosis?

A

Autosomal Recessive.

23
Q

How do you manage Hereditary Haemochromatosis?

A

Venesection (frequent bleeding) to reduce the risk of developing hepatocellular carcinoma.

24
Q

How can Wilson’s disease cause Cirrhosis?

A

There is abnormal copper metabolism as there is reduced secretion of copper from the biliary system so it accumulates in tissues (liver and other organs). As there is more storage there is reduced serum copper and caeruloplasmin. There will be copper deposits on a biopsy. There may be Kayser-Fleishcerring Ring (a ring of copper around the eye).

25
Q

What is the genetic characteristic of Wilson’s disease?

A

Autosomal recessive (even rarer than Hereditary Haemochromatosis).

26
Q

How do you manage Wilson’s disease?

A

Using chelating agens and zinc (which helps the chelating agents). The patient will eventually need a liver transplant.

27
Q

What are the characteristics of Primary Sclerosising Cholangitis?

A

Autoimmune condition.
Fibrosis of the intra- and extra-hepatic bile ducts.
Typically occurs in men.
Can be asymptomatic or present with pruritus (itchy. skin), jaundice or cholangitis (inflammation of the gallbladder).
There is an association with hepatobiliary malignant and ulcerative colitis.
Deranged LFTs suggesting an obstructive picture.
Presence of ANCA antibodies.

28
Q

What are the characteristics of Primary Biliary Cirrhosis?

A

Autoimmune condition.
Destruction of the intra-hepatic bile ducts.
Typically occurs in women.
Can be asymptomatic or present with pruritus +/- jaundice.
Hepatomegaly is present in advance stages of the disease.
Deranged LFTs suggesting an obstructive picture.
Presence of AMAs antibodies.

29
Q

Define Portal Hypertension.

A

A build up of blood in the portal venous system.

30
Q

Describe the pathogenesis of Portal Hypertension.

A

There is a build up of blood in the portal venous system. Fibrotic liver is not very expandable so due to the increased pressure compresses the veins entering the liver from the portal venous system. This causes ascites. Subsequently the blood can shunt from the portal system to the systemic venous circulation . This leads to distension of the veins at the site of anastomoses which are varices (dilated veins).

31
Q

Define ascites.

A

Increased amount of fluid in the peritoneal cavity.

32
Q

Where are 3 clinical relevant anastomosise that can become varices in portal hypertension?

A
  1. Oesophageal.
  2. Umbilical.
  3. Anorecal.
33
Q

How does Oesophageal Varices occur and how does it present?

A

Occurs in the distal portion of the oesophagus. Portal hypertension can lead to mucosal varices, which if they rupture can cause haematemesis (vomiting blood).

34
Q

What is the word for vomiting blood?

A

Haematemesis.

35
Q

How does Umbilical Varices occur in Portal Hypertension and how does it present?

A

The ligamentum trees (a remnant of the umbilical vein) links the liver to the umbilicus. There is usually no blood flow but with increased portal blood pressure this can lead to Caput Medusa (abdominal varices that look like snakes).

36
Q

How does Anorectal Varices occur in Portal Hypertension and how does it present?

A

Between the superior and middle and inferior rectal veins there are anastomosis where varices can occur. This present as haemorrhoids which are typically painless.

37
Q

What is Hepatorenal Syndrome?

A

The development of the Acute Kidney Injury in the presence of cirrhosis. The kidney improves dramatically if the patients liver failure is reversed.

38
Q

Describe the pathogenesis of Hepatorenal Syndrome.

A

There is portal hypertension which causes the splanchnic arteries to vasodilate via Nitric Oxide. This causes RAAS to be activated as it is sensed as a low BP. RAAS constricts the renal artery, reducing blood flow to the kidney. This drops GFR which causes acute kidney injury.

39
Q

Why do Gallstones occur?

A

An accumulation of bile contents (cholesterol, bile pigments and phospholipids) can form gallstones.

40
Q

What is relevant about gallstones in imaging?

A

They are radiolucent so don’t show up on an X-ray (compared to renal calculi which are made from calcium so would show up on an X-ray.

41
Q

Describe Biliary Colic in the context of complications of gallstones.

A

The patient will present with RUQ pain after eating a fatty meal. This is because there is temporary obstruction of a gallstone in the cystic or common bile duct which only obstruct when bile is being released.
The gallstone can be seen on an ultrasound.
The patient will have abnormal LFTs but no features of inflammation.

42
Q

What is the management of Biliary Colic?

A

Analgesia and an elective cholecystectomy (removal of the gallbladder).

43
Q

Describe Acute Cholecystitis in the context of complications of gallstones.

A

Initially presentation very similar to binary colic.
There is impaction of a stone in the cystic duct. It presents with inflammatory signs. Fever and RUQ.
Can be determined with Murphy’s sign (when the person breaths in you can touch the gallbladder with your finger so they cannot breath in all the way).
It is seen on an ultrasound as a thick wall gallbladder.

44
Q

How do you manage Acute Cholecystitis?

A

Initially conservative methods, followed by cholecystectomy.

45
Q

Describe Acute Cholangitis in the context of complications of gallstones.

A

Infection of the biliary tree, presents with RUQ pain and features of inflammation and jaundice (Charcot’s triad). It is typically due to a common bile duct stone or other obstructive cause.

46
Q

How do you manage Acute Cholangitis?

A

IV antibiotics, fluids and relieve the obstruction.

47
Q

Describe Acute Pancreatitis in the context of complications of gallstones.

A

There is acinar cell injury and necrosis which evokes an inflammatory response.
Present with epigastric pain which radiates to the back as the pancreas is a foregut structure that is retroperitoneal . Often associated with vomiting due to severity of pain.
There is Cullen’s sign of bruising at the umbilicus and Grey-Turner’s sign of flank bruising.

48
Q

What are the 3 main causes of Acute Pancreatitis?

A
  1. Gallstones.
  2. Ethanol.
  3. Steroids.
49
Q

What is the pathogenesis of Acute Pancreatitis.

A

Due to necrosis of the pancreas acinar cells there is release of amylase so the pancreas digests itself.

50
Q

How do you diagnosis Acute Pancreatitis?

A

Rule out other causes then do a CT/MRI to identify any necrosis.

51
Q

How do you manage Acute Pancreatitis?

A
  1. Fluids.
  2. Manage gallstones.
  3. Organ support.

Gastrointestinal (10 decks)

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