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3 - GI > Liver and Pancreas Pathology > Flashcards

Liver and Pancreas Pathology Flashcards

1
Q

Describe the process of bilirubin formation and excretion

A
  • Breakdown of red cells occurs extravascularly in macrophages in the spleen and liver
  • Bilirubin released by heme breakdown is hydrophobic and therefore bound to albumin before being carried to the liver
  • In the liver, bilirubin is conjugated with glucuronic acid by UDP glucuronyl transferase
  • Conjugated bilirubin is water soluble and is secreted by hepatocytes into the bile canaliculi
  • Bile then enters the duodenum and converted to urobilinogen
  • 10% of urobilinogen is reabsorbed into the blood and excreted from the kidneys as urobilin
    • Light yellow colour
  • 90% of urobilinogen remains in the intestines and excreted as stercobilin in feces
    - Dark brown colour
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2
Q

Outline the anabolic function of the liver

A
  • Albumin - measured clinically
  • Glycogen
  • Numerous coagulation factors - measured clinically
  • Haematopoiesis in fetus
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3
Q

Outline the catabolic function of the liver

A
  • Drugs - cytochrome P450
  • Hormones
  • Haemoglobin - measured clinically
  • Poisons - cytochrome P450
  • Can take over removal of aged red cells after splenectomy
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4
Q

What tests can be conducted to measure liver function

A
  • Hypoalbuminaemia reflects severe liver dysfunction
  • Prolonged prothrombin time (INR) - failure to produce coagulation factors
  • ALT
  • ALP
  • Gamma GT
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5
Q

What does high ALT show

A
  • Alanine aminotransferase (ALT)
  • Released by inflamed or damaged hepatocytes into blood
  • Raised in hepatitis
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6
Q

What does high ALP show

A
  • Alkaline phosphate (Alk Phos)
  • Enzyme present in the liver canaliculi, bile ducts and bone
  • Normally higher in growing bone - up to 20 years old
  • Raised in liver disease with cholestasis
    • Biliary obstruction, cirrhosis, liver metastases
    • Drugs
  • Raised in bone disease
    • Bone metastases, bone fractures - can compress bile duct
    • Osteomalacia, hyperparathyroidism
    • Paget’s disease of bone - failure to replace old bone with new bone
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7
Q

What does high gamma GT show

A
  • Enzyme present in bile duct cells and some in hepatocytes
  • Raised in bile duct obstruction, cirrhosis, liver metastases, drugs
  • Raised in alcoholism
    • Could be raised in alcoholism with no liver damage
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8
Q

List potential causes of jaundice

A
  • Hepatitis
  • Common bile duct stones
  • Carcinoma of the head of the pancreas
  • Liver metastases
  • Late stages of cirrhosis
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9
Q

Describe pre-hepatic jaundice

A
  • Too much bilirubin production
  • Eg. Haemolytic anaemia (sickle cell anaemia) - breakdown lots of RBC
  • Mild jaundice
  • Urine colour normal but stools may be very dark
  • No pruritis
  • Blood test
    • Raised serum bilirubin
    • Increased urinary urobilinogen
    • No conjugated bilirubin in urine
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10
Q

Describe intra-hepatic jaundice

A
  • Failure of hepatocytes to conjugate and/or secrete most of the bilirubin presented to them
  • Eg. Hepatitis, cirrhosis
  • Partial conjugation - not all excreted into bile
  • Stasis within the liver is called cholestasis - bile stuck in liver
  • Moderate jaundice
  • Stools normal but urine dark
  • No pruritis usually
  • Blood test
    • Raised serum bilirubin
    • Increase in unconjugated bilirubin levels
    • Normal urinary urobilinogen
      • Conjugated bilirubin present in urine
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11
Q

Describe post-hepatic jaundice

A
  • Failure of the biliary tree to convey the conjugated bilirubin to the duodenum
  • Eg. Biliary tree obstruction
  • Inability to secrete bile salts leads to itching (pruritis)
  • Severe jaundice
  • Stools pale and urine dark
  • Blood test
    • Raised serum bilirubin
    • Decreased urinary urobilinogen - as bilirubin does not enter GI system
    • Conjugated bilirubin present in urine
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12
Q

How is conjugated bilirubin seen in urine

A
  • Conjugated bilirubin is water soluble - if levels are high in blood, then it will be excreted in urine
  • Turns the urine a dark yellow colour
  • Can be measured with a dipstick
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13
Q

State causes of hepatitis

A
  • Viral - hepatitis A, B, C
  • Acute alcohol intake
  • Fatty liver disease - obesity leading to fat deposition and cirrhosis
  • Drugs/toxins
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14
Q

Describe consequences of liver failure

A
  • Increased susceptibility to infections - mostly bacterial
  • Increased susceptibility to toxins and drugs
  • Increased blood ammonia due to failure to clear ammonia via urea cycle
    • Produced by colonic bacteria and deamination of amino acids
    • Causes hepatic encephalopathy - neuropsychiatric abnormalities due to liver disease
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15
Q

What would be see on a blood test for hepatitis

A
  • Very high serum ALT
  • High serum bilirubin
  • Normal albumin and INR
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16
Q

Describe the consequences and progression of alcoholic liver disease

A
  • Alcoholic fatty liver disease -> alcoholic hepatitis -> cirrhosis
  • Damage to liver greater than its ability to regenerate
  • Can lead to internal bleeding, build up of toxins in the brain (encephalopathy), ascites, liver cancer
17
Q

Describe the consequences of liver cirrhosis

A
  • Pressure and occlusion of the hepatic sinusoids
    • Leads to portal hypertension which leads to portosystemic shunting (bypass liver in circulation)
  • Pressure on the bile canaliculi and therefore reduced ability to excrete toxins, bilirubin
  • Replacement of hepatocytes by fibrous tissue which leads to reduced albumin and clotting factor production
18
Q

What are symptoms of liver cirrhosis

A
  • Fatigue/weakness
  • Bleeding and bruising easily
  • Ascites
  • Swollen legs - hypoproteinaemia
  • Weight loss
  • Jaundice
  • Haematemesis and or melaena
  • Confusion, drowsiness, slurred speech - hepatic encephalopathy
19
Q

Outline how liver diseases may lead to portal hypertension and appreciate the associated pathology these may lead to

A
  • Hepatic sinusoids are a low pressure system
    • Inflammation due to hepatitis can block sinusoids or bile ducts, thus increasing pressure
    • Hepatic arteries have high pressure so not normally compromised
  • Increase in pressure in the hepatic sinusoids causes increase in portal vein pressure
  • Leads to ascites due to increased hydrostatic pressure within the portal veins
20
Q

Describe the blood test seen on gallstones

A
  • Serum bilirubin very high

- Raised Alk Phos and gamma GT

21
Q

Why do gallstones form

A
  • Gallstones develop in the gallbladder as a result of chemical imbalances in the bile
  • 80% due to excess cholesterol crystallizing and growing to form stones
  • 20% due to gallstones forming from excess levels of bilirubin
22
Q

Describe what a biliary colic is

A
  • Pain in the right upper quadrant that radiates to the tip of the right scapula/right shoulder
  • Due to lodged gall stone in the cystic duct
  • Often precipitated by eating a fatty meal
  • Lasts up to 6 hours
  • Not a true colic - colic is intermittent pain due to muscular contractions attempting to move past an obstruction
23
Q

What is acute cholecystitis

A
  • Inflammation of the gall bladder
  • If a gallstone obstructs the cystic duct, then there is stasis of the gallbladder contents - infection risk
  • E. Coli normally infecting organism
  • Presents with severe gall bladder pain and also is systemically unwell
24
Q

What would be seen on a blood test for liver metastases

A
  • Raised Alk Phos
  • Raised serum bilirubin
  • Conjugated bilirubin present in urine
25
Q

Describe the causes of acute pancreatitis

A
  • Alcohol - increases zymogen secretion from acinar cells and decreases bicarbonate and fluid from the ducts
    • Pancreatic juices become thick, which can form a plug and block the duct
    • Leads to auto-digestions and cell destruction
  • Gallstones - gallstone at the sphincter of oddi can block pancreatic secretions and activates zymogens
26
Q

Describe the pathogenesis of acute pancreatitis

A
  • Acute pancreatitis due to premature activation of pancreatic proteases in the pancreas
  • Proteases auto-digest the pancreas and the retroperitoneum
27
Q

Describe the blood test for acute pancreatitis

A
  • Raised serum amylase or serum lipase

- CT scan may be used in moderate/severe cases to look for pancreatic necrosis/pseudocyst

28
Q

Describe the treatment for acute pancreatitis

A
  • No specific treatment

- Analgesia (pain relief) - fluid resuscitation needed as patients lose many litres of fluid in their retroperitoneum

29
Q

Describe the causes and consequences of chronic pancreatitis

A
  • Chronic pancreatitis due to repeated low grade pancreatitis that causes pancreatic fibrosis
  • Due to alcohol abuse, cystic fibrosis, tumours
    • Cystic fibrosis - pancreatic secretions become thick and sticky
  • Pancreas becomes calcified and patients suffer severe epigastric and back pain that leads to opiate addiction
  • Both exocrine and endocrine gland fail due to fibrosis
30
Q

Describe the presentation of carcinoma of the pancreas

A
  • Anorexia, malaise, fatigue
  • Significant weight loss
  • Epigastric and/or back pain
  • Dark urine, pale stools, pruritis - can be due to bile duct obstruction

3 - GI (14 decks)

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