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GI tract > Liver pathology > Flashcards

Liver pathology Flashcards

1
Q

What are the functions of the liver?

A
  • Storage
  • Synthetic
  • Metabolic
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2
Q

What is stored in the liver?

A
  • Glycogen
  • Vitamins
  • Iron
  • Copper
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3
Q

What is synthesised by the liver?

A
  • Glucose
  • Lipids/cholesterol
  • Bile
  • Clotting factors
  • Albumin (main protein in systemic circulation)
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4
Q

What is the metabolic function of the liver?

A
  • Detoxifying
  • Bilirubin
  • Ammonia
  • Drugs
  • Alcohol
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5
Q

What are the symptoms of liver pathology?

A
  • Jaundice
  • Oedema/ascites
  • Bleeding
  • Confusion
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6
Q

Why does liver pathology cause jaundice?

A
  • Bilirubin not conjugated by the liver
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7
Q

Why does liver pathology cause oedema/ascites?

A
  • Reduced ability of liver to synthesise albumin
  • Leads to reduced oncotic pressure in the blood
  • Water leaves circulation and cannot be drawn back from interstitium
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8
Q

Why does liver pathology lead to bleeding?

A
  • Reduced clotting factor production
  • Happens over a long period of time unless damage is extreme
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9
Q

Why does liver pathology lead to confusion?

A
  • Impaired ammonia detoxification
  • Ammonia is soluble + diffuses across blood brain barrier
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10
Q

What are the initial symptoms of liver pathology?

A
  • Fatigue
  • Nausea
  • Abdominal pain
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11
Q

What can cause acute liver pathology?

A
  • Alcohol
  • Paracetamol
  • Viruses (EBV, CBV)
  • Medications e.g. aspirin in children
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12
Q

What is the difference between decompensated liver disease and acute liver failure?

A
  • If jaundice, oedema/ascites, bleeding and confusion happen acutely = decompensated liver disease
  • If this occurs without any history of liver disease = acute liver failure
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13
Q

What is cirrhosis?

A
  • Permanent irreversible damage to liver resulting in impairment of function and distortion of liver architecture due to chronic inflammation
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14
Q

Outline how alcoholic liver disease causes a fatty liver

A
  • Usually reversible
  • Alcohol releases glucose as it’s broken down
  • Insulin causes glucose to be stored as starch
  • But if there’s an excessive amount it is stored as triglycerides
  • Fatty deposits build up in the liver
  • Large liver due to fat
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15
Q

Which drugs can cause liver inflammation?

A
  • Iatrogenic drugs that become hepatotoxic
  • Alcohol (alcoholic liver disease)
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16
Q

How does alcoholic liver disease progress?

A
  • Fatty change (weeks) causes hepatomegaly
  • Alcoholic hepatitis (years) causes right upper quadrant pain and jaundice
  • Cirrhosis
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17
Q

Outline alcoholic hepatitis

A
  • See inflammation and inflammatory cells in liver
  • More severe symptoms
  • Jaundice, RUQ pain, hepatomegaly, oedema, ascites
  • Initially reversible but can become permanent if cirrhosis occurs
  • Treat symptoms and reduce alcohol intake
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18
Q

Outline alcoholic hepatitis

A
  • See inflammation and inflammatory cells in liver
  • More severe symptoms
  • Jaundice, RUQ pain, hepatomegaly, oedema, ascites
  • Initially reversible but can become permanent if cirrhosis occurs
  • Treat symptoms and reduce alcohol intake
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19
Q

Which infections can cause inflammation of the liver?

A
  • Hepatitis B - vaccine, no cure, symptomatic
  • Hepatitis C - IV drug use, cure, no vaccine, asymptomatic
  • Hep C can lead to malignancy
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20
Q

What is NAFLD?

A
  • Non-alcoholic fatty liver disease
  • Insulin resistance
  • Triglycerides accumulate in hepatocytes
  • Cause inflammation
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21
Q

What is NASH?

A
  • Non-alcoholic steatohepatitis
  • inflammation
  • more present due to obesity and diabetes
  • Treat symptoms and reduce risk factors e.g. blood glucose levels
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22
Q

What is hereditary haemochromatosis and how does it affect the liver?

A
  • Autosomal recessive
  • Linked to increased ferritin levels
  • Increased absorption of iron from small intestine
  • Increased deposition in the liver
  • Causes inflammation
  • Treated with venesection
23
Q

What is Wilson’s disease and how does it affect the liver?

A
  • Decreased copper secretion from biliary system into circulation for removal
  • Increased deposition of caeruloplasmin in blood
  • Pt will ultimately need liver transplant
  • Causes seizures, tremors and memory problems
24
Q

What are the autoimmune causes of liver inflammation?

A
  • Autoimmune hepatitis - hepatocytes are attacked by the autoantibodies ASMA and ANA
  • Primary biliary cirrhosis due to autoantibody AMA
  • Primary sclerosing cholangitis
25
Q

What are the other causes for liver inflammation?

A
  • Alpha antitrypsin
  • Glycogen storage disease
  • Budd-Chiari
26
Q

What does the inferior mesenteric vein drain?

A
  • Descending colon
  • Drains into splenic vein
  • Joins with SMV to make portal vein
27
Q

What does the superior mesenteric vein drain?

A
  • Ascending colon
28
Q

What is portal hypertension?

A
  • Main complication of cirrhosis
  • Build-up of blood in portal venous system
29
Q

Why does portal hypertension occur?

A
  • Fibrotic tissue accumulates
  • Liver less expansive
  • Needs to be expansive because venous drainage from majority of GI tract passes through
30
Q

Why does portal hypertension lead to ascites?

A
  • Fibrosis compresses veins
  • Increase in hydrostatic pressure in portal venous system
  • Fluid leaks out
  • Ascites
31
Q

Why does portal hypertension lead to splenomegaly?

A
  • Leads to increased pressure in splenic circulation
32
Q

Why does portal hypertension cause varices?

A
  • Increased pressure in portal circulation
  • Blood shunts from portal circulation to systemic circulation
  • Normally there are anastomoses between the 2 circulations, but these should not contain any blood
  • Increased pressure in portal circulation causes distension of veins at these anastomoses
33
Q

Outline oesophageal varices?

A
  • Superior 2/3 drain into oesophageal veins and then to superior vena cava
  • Distal 1/3 drains into left gastric vein and then to portal vein
  • At junction there is crossover of veins where pressure can build
  • Veins are superficial and fragile
  • When they get dilated they are liable to rupture
  • Causes significant haematemesis
  • Can be life-threatening
34
Q

Where can varices occur in the body?

A
  • Oesophagus
  • Anorectal
  • Umbilicus
35
Q

Outline ano-rectal varices

A
  • Occurs between superior rectal vein and middle and inferior rectal veins
  • Typically painless because they’re above the pectinate line
  • Rarey bleed
36
Q

Outline umbilical varices

A
  • Less common
  • Only occur if portal hypertension is severe
  • Ligamentum teres (should be non-functional in adults) connects abdominal wall and circulation
  • Caput medusa sign - pattern of superficial veins on abdominal wall
37
Q

What is hepatorenal syndrome?

A
  • Failing liver leads to failing kidneys
  • Kidney deterioration is acute and rapid
38
Q

Outline what happens to result in hepatorenal syndrome

A
  • Portal hypertension backlogs through venous system
  • Affects arterial circulation coming in (splanchnic)
  • Vasodilation of splanchnic arteries to reduce pressure in system
  • Perceived as decreased circulating volume because blood is stuck in portal system
  • RAAS is activated
  • Renal artery vasoconstriction occurs
  • Decreased perfusion
  • Reduced kidney function
39
Q

Outline the flow of the bile ducts

A
  • Bile ducts in liver coalesce
  • Form left and right hepatic duct
  • Left and right hepatic duct form common hepatic duct
  • Cystic duct from gall bladder joins with common hepatic duct
  • Forms common bile duct
40
Q

What is the name of the site where the common bile duct and the pancreatic duct empty?

A
  • Ampulla of Vater
  • Sphincter of Oddi controls rate of release
41
Q

What is biliary colic?

A
  • Constant pain lasting for a few hours and then easing
  • Gallstones cause sudden onset RUQ pain immediately after eating a large fatty meal
42
Q

What causes biliary colic?

A
  • CCK is released after eating a large fatty meal
  • CCK release causes gallbladder to contract
  • Gallstone is pushed up against neck of gallbladder
  • Causes temporary obstruction to cystic duct and pain
  • No inflammation
43
Q

How is biliary colic treated?

A
  • Give pain relief
  • Plan operation to remove gallbladder
44
Q

What is acute cholecystitis?

A
  • RUQ pain
  • Gallstone impacted in cystic duct so nothing can pass through
  • Inflammation
  • Positive Murphy’s sign
45
Q

What is Murphy’s sign?

A
  • Place hand on right side of liver
  • Ask patient to take a deep breath in
  • Gallbladder is pushed down and hits hand
  • Causes intense pain
  • Patient will inhale sharply
46
Q

What is ascending cholangitis?

A
  • Infection of biliary tree
47
Q

What are the symptoms of ascending cholangitis?

A

Charcot’s triad:
1. RUQ pain
2. Inflammation
3. Jaundice

48
Q

What causes ascending cholangitis?

A
  • Happens when stone reaches common bile duct
  • Causes stasis above point of blockage
  • Causes infection behind stone
  • Give antibiotics, fluids, surgical removal
49
Q

What forms gallstones?

A
  • Cholesterol
  • Bile pigments
  • Mixed
50
Q

What are the risk factors for gallstones?

A
  • Diet
  • Female
  • Forties
  • Pregnancy
51
Q

How are gallstones picked up on imaging?

A
  • Ultra-sound scan
52
Q

What leads to acute pancreatitis?

A
  • Stone in common bile duct either at or after point at which pancreatic duct joins
  • Causes complete obstruction of bile and enzymes of pancreas
  • Auto-digestion
53
Q

What are the symptoms of pancreatitis?

A
  • Epigastric pain that goes to the back
  • Vomiting
  • Cullen’s and Grey-Turner’s
  • Amylase and lipase increase in the blood
54
Q

How do we diagnose pancreatitis?

A
  • Look for raised amylase and lipase in the blood
  • CT/MRI to look for inflammation
  • Give lots of fluids for organ support

GI tract (23 decks)

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