GI11 - Liver & Biliary System Pathology Flashcards

1
Q

3 main functions of the liver

Storage x4
Synthesis x7
Metabolism x6

A

1.) Storage - glycogen, vitamins, iron, copper

2.) Synthesis - bile, lipids, cholesterol, glucose, protein, coagulation factors, albumin

3.) Metabolism - alcohol, drugs, bilirubin, ammonia, carbohydrates, lipids

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2
Q

5 symptoms of liver disease

General Symptoms
4 Specific Symptoms (and causes)

A

1.) General Symptoms - nausea/vomiting, fatigue, anorexia, abdominal pain

2.) Jaundice - deranged bilirubin metabolism

3.) Oedema/Ascites - deranged albumin synthesis

4.) Bleeding/Easy Bruising - deranged clotting factor synthesis

5.) Confusion - deranged ammonia metabolism

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3
Q

3 causes of acute liver failure

A

1.) Drug Overdose/Medication - e.g. paracetamol, tetracycline, aspirin in children

2.) Acute Viral Infections - EBV, CMV, Hep A/B

3.) Acute Excessive Alcohol Intake

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4
Q

4 features of liver cirrhosis

Cause
Reversibility
Liver Function
Architecture

A

1.) Chronic Liver Disease - develops in response to any chronic liver injury
- inflammation –> fibrosis –> hepatocyte necrosis

2.) Irreversible - end result of a lot of conditions

3.) Impaired Liver Function - less functional hepatocytes

4.) Distortion of Architecture - hard nodules on liver

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5
Q

5 groups of causes of liver cirrhosis (chronic liver disease)

Drugs
Infection
Deposition x3
Autoimmune x3
Others x3

A

1.) Drugs - alcoholic liver disease, iatrogenic

2.) Infection - chronic Hep B or C
- Hep B has a vaccine but no cure, symptoms during acute infection
- Hep C has a cure but no vaccine, most asymptomatic during acute infection
- risk of hepatocellular carcinoma

3.) Deposition - fat, iron, copper
- non-alcoholic fatty liver disease (fat)
- hereditary haemochromatosis (iron)
- Wilson’s disease (copper)

4.) Autoimmune - autoimmune hepatitis, primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC)
- autoimmune hepatitis affects hepatocytes
- PBC and PSC affects the bile duct

5.) Others - alpha-1 antitrypsin deficiency, glycogen storage, Budd-Chiari

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6
Q

5 features of alcoholic liver disease

What is it?
Mechanism
Fatty Change
Alcoholic Hepatitis
Cirrhosis

A

1.) Liver damage caused by chronic exposure to alcohol

  1. Mechanism - build up in acetyl CoA
    - increased fatty acid synthesis
    - decreased lipoprotein synthesis (less removal of lipids)

3.) Fatty Change - occurs after weeks, initially reversible
- also causes hepatomegaly

4.) Alcoholic Hepatitis - after years, initially reversible
- inflammation occurs, neutrophils present
- rapid onset of jaundice, tender hepatomegaly (RUQ)
- also get nausea, oedema and ascites, splenomegaly

5.) Cirrhosis - end stage, irreversible damage
- hepatocyte necrosis, nodules

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7
Q

3 features of non-alcoholic fatty liver disease

Pathogenesis
Inflammation
Common Causes x4

A

1.) Pathogenesis - similar to alcoholic liver disease
- accumulation of lipids in hepatocytes
- however, alcohol isn’t involved, theres a link to insulin resistance

2.) Inflammation Present - called Non-Alcoholic Steatohepatitis (NASH)

3.) Common Causes - obesity, diabetes, metabolic syndrome, familial
hyperlipidaemia

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8
Q

Iron and copper deposition in causing cirrhosis

Hereditary Haemachromatosis
Wilson’s Disease

A

1.) Iron - hereditary haemochromatosis
- mutated HFE doesn’t reduce the affinity for the transferrin receptor for iron-bound transferrin
- negative influence on iron uptake is lost which leads to iron accumulation in cells (increased ferritin)
- increases risk of hepatocellular carcinoma

2.) Copper - Wilson’s Disease
- reduced secretion of copper from biliary system leads to accumulation of copper in tissues
- have low caeruloplasma

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9
Q

5 complications of cirrhosis

Portal Hypertension
Ascites
Splenomegaly
Varices
Hepatorenal Syndrome

A

1.) Portal Hypertension - fibrotic liver is not expansive so build up of blood in portal venous system
- compresses veins entering the liver from portal system
- underlying cause of other complications

2.) Ascites - accumulation of fluid in the peritoneal cavity
- portal hypertension -> high HP in portal venous system
- less albumin produced –> decreased oncotic pressure
- net movement of fluid into peritoneal cavity

3.) Splenomegaly - enlarged spleen
- pressure build up in splenic circulation

4.) Varices - distension of veins at site of anastomoses
- high pressure causes blood to ‘shunt’ from the portal system to the systemic venous circulation
- uses anastomoses that aren’t used in normal condition

5.) Hepatorenal Syndrome - development of acute kidney injury (AKI) in the presence of cirrhosis
- reduced blood flow to the kidney
- portal hypertension –> arterial vasodilation –> activation of RAAS –> renal artery vasoconstriction

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10
Q

3 important sites of varices

A

1.) Oesophageal Varices
- upper 2/3 of portal vein drains into oesophageal veins
- can lead to mucosal varicies
- can cause haematemesis (vomiting blood) if it ruptures

2.) Anorectal Varices
- between superior and middle/inferior rectal veins
- typically painless above the pectinate line
- rarely bleed

3.) Umbilical Varices - rare
- ligamentum teres links liver to the umbilicus
- there is normally no blood flow

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11
Q

The Biliary Tree

A

1.) Common Hepatic Duct - duct from the liver
- made up by the right and left hepatic duct

2.) Cystic Duct - duct from the gallbladder

3.) Common Bile Duct - common hepatic + cystic duct
- pancreatic duct also joins distally
- enters the duodenum at the Ampulla of Vater

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12
Q

4 features of gallstones

Contents
Risk Factors (5Fs)
Complications x4
Imaging

A

1.) Contents - formed from bile contents (cholesterol, bile pigments)

2.) Risk Factors - 5 Fs
- Fat, Female, Forty, Fertile, Family History
- others: pregnancy, oral contraceptives (oestrogen ↑ cholesterol in bile), malabsorption
- haemolytic anaemia (causes pigmented gallstones)

3.) Complications - biliary colic, acute cholecystitis, acute ascending cholangits, acute pancreatitis

4.) Imaging - use ultrasound
- most are radiolucent so can’t been seen on x-rays
- kidney stones can be seen on x-rays though

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13
Q

4 complications of gallstones

Biliary Colic
Acute Cholecystitis
Acute Ascending Cholangitis
Acute Pancreatitis

A

1.) Biliary Colic - RUQ pain due to temporary obstruction of a gallstone in the cystic duct
- occurs after eating a fatty meal because CCK release causes the gallbladder to contract against a blockage
- no features of inflammation

2.) Acute Cholecystitis - RUQ pain due to permanent obstruction of a gallstone in the cystic duct
- seen on ultrasound (thick gallbladder wall)
- Murphy’s sign positive

3.) Acute Ascending Cholangitis - RUQ pain due to permanent obstruction in the common bile duct
- infection of the biliary tree
- Charcot’s traid: pain, inflammatory features, jaundice
- can also get hypotension and confusion
- management: IV antibiotics, fluids, relieve obstruction

4.) Acute Pancreatitis - epigastric pain due to blockage of the pancreatic duct, often associated with vomiting
- release of pancreatic enzymes causes autodigestion of pancreatic cells, evoking an inflammatory response
- pain can radiate to the back
- Cullen’s (bruising around umbilicus) and Grey Turner’s (bruising of the flank) sign
- management: fluids, remove gallstones, organ support

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