Liver And Biliary Pathology Flashcards

1
Q

What are the normal functions of the liver?

A

Storage - glycogen, vitamins, iron, copper
Synthesis - glucose, protein, lipids and cholesterol, bile, coagulation factors, albumin
Metabolism / detoxification - Bilirubin, Ammonia, drugs, alcohol, carbohydrates and lipids

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2
Q

What is cirrhosis?

A

Cirrhosis is an irreversible state that occurs in the liver due to chronic inflammation.

  • Ongoing inflammation causes fibrosis
  • Associated with hepatocyte necrosis
  • Resulting architectural changes - nodules

NON-REVERSIBLE

End result is:
-Imparment of liver function and distortion of architecture leads to vascular changes (portal hypertension)

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3
Q

What can cause cirrhosis?

A

Drugs - alcohol, iatrogenic

Infection - HBV, HCV

Deposition - fat, iron, copper

Autoimmune - autoimmune, hepatitis, PBC, PSC

Other - a1-antitrypsin, glycogen storage, Budd Chiari

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4
Q

What are the three main mechanisms in which alcohol can affect the liver?

A

Fatty change - reversible (weeks)

Alcoholic hepatitis - initially reversible (years)

Cirrhosis - end stage, irreversible damage (years)

Thought to be partly due to the build up of acetaldehyde.

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5
Q

What can a fatty liver cause?

A

Hepatomegaly

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6
Q

What are the symptoms of alcoholic hepatitis?

A

Can be asymptotic.

Rapid onset jaundice, tender hepatomegaly (RUQ pain)

Symptoms of more severe disease e.g. nausea, oedema, ascites, splenomegaly

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7
Q

How does viral hepatitis cause cirrhosis?

A

Chronic hep B or C

Blood blown virus

Also poses risk for hepatocellular carcinoma.

Hep B - vaccine but no cute

Hep C - cure but no vaccine. (Most asymptomatic during acute infection so spreads easily)

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8
Q

What is non-alcoholic fatty liver disease (NAFLD)?

A

Similar pathogenesis to alcoholic liver disease but without alcohol.

Accumulation of triglycerides and other lipids in hepatocytes.

It is becoming more prevalent:

  • Obesity
  • Diabetes
  • Metabolic syndrome

To stop it occurring you should reduce his factors and modify your lifestyle.

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9
Q

What is hereditary haemochromatosis?

A

Abnormal iron metabolism

-Increased absorption of iron from the small intestine —> excess deposition.

Can effect liver and other organs

Elevated serum iron and ferritin levels

Abnormal LFTs

Autosomal recessive (rare)

Treat with venesection

If you have it, there is an increased risk of hepatocellular carcinoma.

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10
Q

What is Wilson’s disease?

A

Abnormal copper metabolism

Very very rare and autosomal recessive

-Reduced secretion of copper from biliary system -> accumulation in tissue
-Can affect the liver and other organs
-Reduced serum copper and caruloplasmin
Copper deposits on biopsy

Treat - chelating agents (get rid of copper), zinc, liver transplant.

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11
Q

What is primary sclerosis cholangitis?

A

Fibrosis of intra and extra hepatic bile dicts

Typically affects men

Can be asymptomatic or present with pruritus, jaundice or cholangitis

Association with hepatobiliary malignancy and UC

Deranged LFTs (obstructive picture) and presence of antibodies (ANCA)

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12
Q

What is primary biliary cirrhosis?

A

Destruction of intrahepatic bile ducts.

Typically affects women

Can be asymptomatic or present with pruritus +/-jaundice and may have other conditions (RA)

Hepatomegaly in advanced disease.

Deranged LFTs (obstructive picture) and presence of antibodies (AMAs)

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13
Q

What is portal hypertension?

A

Build up of blood in the portal venous system.

  • Fibrotic liver is not very expandable
  • Compresses veins entering the liver from the portal venous system.
  • This causes increased hydrostatic pressure in the portal venous system.
  • Cases ascites
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14
Q

How can portal hypertension cause varices?

A

Blood can shunt from the portal system to the systemic venous circulation.

This leads to distention of the veins at the site of the anastomoses -varices

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15
Q

What are the three important sites of varices?

A

Oesophagus -These are the most worrying!

  • The distal portion of the oesophagus
  • Can lead to mucosal varices
  • If these rupture, it can cause significant haematemisis (vomitting blood - worrying)

Umbilical

  • Ligament teres links the liver to the umbilicus
  • Normally no blood flow
  • Caput medusa

Anorectal
- Between superior and middle and inferior rectal veins
Haemorrhoids - typically painless.

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16
Q

Describe how AKI develops in the presence of cirrhosis.

A

Portal hypertension

Arterial vasodilation (splanchnic)

RAAS activated

Renal artery vasoconstriction (reduced blood flow to kidney)

17
Q

What forms gallstones?

A

Cholesterol
Bile pigments
Phospholipids

Most are radiolucent - comparison to renal calculi

18
Q

What is biliary colic?

A
  • RUQ pain
  • Temporary obstruction of a gallstone in the cystic duct or common bile duct
  • See on US
  • Might have abnormal LFTs
  • No features of inflammation

It is contraction of gallbladder against obstruction.

management - analgesia, Cholecystectomy

19
Q

What are the complications of gallstones?

A

Biliary colic

Acute cholecystitis

Acute ascending cholangitis

20
Q

What is acute cholecystitis?

A

Initial presentation very similar to biliary colic

Impactation of a stone in system duct

Inflammatory features

Murphy’s sign - inflamed gallbladder touches finger and causes pain

Seen on US - thick gallbladder

Management - initially conservative then cholecystectomy

21
Q

What is acute cholangitis?

A

Infection of the biliary tree

Present with pain, features of inflammation and jaundice “Charcot’s Triad”

Typically due to a CBD stone or other obstructive cause.

Management - IV antibiotics, fluids, relive obstruction

22
Q

What is acute pancreatitis?

A

Acinar cell injury and necrosis

Evokes an inflammatory response

Presentation:

  • Radiates to back
  • Epigastric pain
  • Often associated with vomitting
  • Cullen’s and Grey Turner’s sign

Release of pancreatic enzymes: amylase
Rule out other causes: CT/MRI to identify necrosis

Management depends on severity:

  • Fluids
  • Manage gallstones
  • Organ support