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MD3002 > Hepatobiliary and pancreatic disease > Flashcards

Hepatobiliary and pancreatic disease Flashcards

1
Q

What are the levels of bilirubin in jaundice ?

A

bilirubin >40μmol/L

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2
Q

Identify the main symptoms of jaundice.

A

-Yellowing of skin and mucosal
surfaces
-Can cause intense itch (because irritates nerve endings in skin)

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3
Q

Is jaundice also present in liver disease ? Is liver disease the only cause of jaundice ?

A
  • Jaundice not always present in liver disease, even when severe
  • Liver disease is not the only cause
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4
Q

Identify the main types of jaundice, and their cause.

A
  • Unconjugated – water-insoluble (bilirubin has not been through liver) → will not pass in urine
  • Conjugated – water-soluble (can be excreted in urine) → dark urine
  • Prehepatic – haemolysis → release of bilirubin from RBCs (more likely to be unconjugated hyperbilirubinemia, because has not been through liver)
  • Intrahepatic – liver disease → excess bilirubin in liver and bloodstream (mixed picture conjugated and unconjugated)
  • Post-hepatic (Obstructive) – obstruction of bile outflow → dark urine and pale stools (mainly conjugated, has been through liver)
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5
Q

Identify the main causes of acute liver injury.

A
  • Viral Infections
  • Alcohol
  • Adverse drug reactions
  • Biliary obstruction (gallstones) causing backflow of bile into liver
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6
Q

Identify the main effects of acute liver injury.

A
  • Jaundice, malaise
  • Raised serum bilirubin and transaminases
  • Liver failure - ↓albumin, ascites (increased inta-abdominal P), bruising (not synthesizing clotting factors), encephalopathy (not breaking down ammonia and products from GI tracts, which then cross BBB and cause neurological symptoms)
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7
Q

Identify the main alcoholic liver injuries.

A
  • Steatosis (not breaking down fat from GI tract, which eventually damages hepatocytes), which may lead to:
  • Acute hepatitis with Mallory’s hyaline, which may lead to:
  • Cirrhosis (but cirrhosis can also happen without previous two)
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8
Q

Define steatosis.

A

“The process describing the abnormal retention of lipids within a cell or organ”, leading to alteration in the metabolism

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9
Q

Define Mallory’s hyaline.

A

“an eosinophilic cytoplasmic inclusion, alcoholic hyalin, found in the liver cells.”

Builds up due to hepatocyte damage (e.g. due to fat build up)

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10
Q

Identify the macroscopic changes leading to alcoholic liver injury.

A
  • Acetaldehyde (breakdown product of alcohol processing) binds to hepatocytes causing damage → Inflammatory reaction
  • Inflammation → fibrosis (since inflammation always recruits fibro and myofibroblasts to heal the area, resulting in fibrosis (prevents infection to spread), which surround nodules.
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11
Q

How does cirrhosis come about ?

A

Fibrosis (collagen) surrounding nodules + Regeneration → Cirrhosis

Fibrosis in liver contracts, around blood vessels, leading to portal hypertension (squeezing portal circulation), which may lead to caput medusae

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12
Q

Identify the main causes of cirrhosis.

A

Anything cause acute liver injury can cause cirrhosis

  • Alcohol
  • Hepatitis B and C viruses
  • Gall stones
  • Auto-immune liver disease
  • Iron overload
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13
Q

Identify the main types of cirrhosis morphologically.

A
  • Micronodular – nodules ≤ 3mm
  • Macronodular – nodules > 3mm
  • Mixed (usually)
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14
Q

Identify the main types of cirrhosis aetiologically.

A
  • Viral hepatitis leading to cirrhosis
  • Due to alcohol use
  • Due to drug use
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15
Q

Identify possible complication of cirrhosis.

A
  • Liver Failure – hepatic encephalopathy (ammonia not broken down anymore, goes into BBB and causes this), build up of steroid hormones (no longer broken down by liver) which results in hyperoestrogenism (palmar erythema and gynaecomastia), bleeding (not synthesizing clotting factors)
  • Portal hypertension –↑ hepatic vascular resistance (due to fibrosis around vessels), AV (between arteries and veins) shunting – oesophageal varices, haemorrhoids, caput medusae
  • Hepatocellular carcinoma (anything that causes cirrhosis, make you more vulnerable to this)
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16
Q

What proportion of all drug reactions involve the liver ?

A

10%

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17
Q

Identify possible drug induced liver injuries.

A

• Injury to liver cells (hepatocellular) – paracetamol overdose
• Injury to bile production/secretion cells
(cholestatic) – methyl testosterone

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18
Q

True or false: Always take a full drug history from a patient with deranged LFTs! (both illicit drug use, and medications)

A

True

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19
Q

What is the main cause of acute biliary obstruction ? What are the symptoms of it ?

A

Gallstones

  • Causes colicky pain and jaundice (back up of bile into liver, mainly conjugated because post-hepatic)
  • Can be complicated by infection of the blocked CBD - cholangitis (medical emergency, needs treatment with antibiotics)
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20
Q

How does chronic liver disease come about ?

A
  • Can follow a clinically evident episode of acute liver injury
  • May have insidious onset without symptoms until later stages
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21
Q

What is a possible clinical result of chronic liver disease ?

A

• Many forms culminate in cirrhosis

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22
Q

Define chronic hepatitis. How may this be diagnosed ?

A

Hepatitis (inflammation of liver) lasting more than 6 months.

Sustained elevation of transaminases (AST, ALT on blood tests) – require liver biopsy to classify cause

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23
Q

Identify the main causes of chronic hepatitis.

A
  • Viral
  • Alcohol
  • Drugs
  • Autoimmune
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24
Q

Identify the main types of chronic Hepatitis.

A
  • Type – aetiology
  • Grade – degree of inflammation
  • Stage – degree of fibrosis
25
Q

Explain the main patterns of hepatocyte injury.

A

Cells closest to central vein (i.e. in zone 3) relatively hypoxic. if toxin injuring them, much less reserve to survive that. In toxic, or haemodynamic injury (e.g. BP not providing enough blood to liver) those are more likely to die off first. Therefore, in acute liver injury, zone 3 most affected.

If auto-immune hepatitis, auto-antibodies by plasma cells get into liver through bloodstream, so those cells closest to bloodstream (i.e. in zone 1) are most affected

26
Q

Identify the main types of chronic hepatitis.

A

1) Non-alcoholic steatohepatitis / Non- alcoholic fatty liver disease
2) Autoimmune Chronic Active Hepatitis

27
Q

Describe the causes, and consequences of NASH / NAFLD.

A
  • Associated with Metabolic Syndrome (DM II, hypertension, ↓HDL cholesterol, ↑ triglycerides), i.e. more prevalent in obese patients
  • Fat deposition in hepatocytes – can lead to cirrhosis (histologically, looks very similar to alcoholic liver disease)
28
Q

Autoimmune Chronic Active Hepatitis

  • Epidemiology
  • Time of onset
  • Pathogenesis
  • Treatment
A

Autoimmune Chronic Active Hepatitis
-Epidemiology: Females > Males
-Time of onset: Usually presents in mid to late teens
-Pathogenesis:
• Interface hepatitis (interface between bloodstream and main hepatic surface)
• Plasma cells (produce the antibodies) and swollen hepatocytes
• Fibrosis
• Anti-Nuclear Antibodies (ANAs), Smooth Muscle Antibodies (SMAs), raised serum IgG and transaminases, anti-LKM (liver-kidney microsomal)

-Treatment: Patients may benefit from steroids

29
Q

Distinguish between Primary Biliary Cholangitis, and Primary Sclerosing Cholangitis:

  • Age/Gender
  • Disease Associations
  • Serum Immunoglobulins
  • Autoantibodies
  • Cholangiography
  • Bile duct injury
  • Portal inflammation
  • Obliterative fibrosis of larger ducts
  • Periportal copper
A

PRIMARY BILIARY CHOLANGITIS

  • Age/Gender: >50, not children, F > M
  • Disease Associations: Other AI diseases (Sjogrens, thyroid)
  • Serum Immunoglobulins: Increased IgM
  • Autoantibodies: AMA, ANA (centromeric)
  • Cholangiography: Normal extrahepatic and large ducts
  • Bile duct injury: Small ducts
  • Portal inflammation: Prominent
  • Obliterative fibrosis of larger ducts: Absent
  • Periportal copper: Present

PRIMARY SCLEROSING CHOLANGITIS

  • Age/Gender: Wide age range, M > F
  • Disease Associations: IBD - UC
  • Serum Immunoglobulins: No significant increase
  • Autoantibodies: None specific, AMA rare
  • Cholangiography: Stricturing and beading
  • Bile duct injury: Large ducts
  • Portal inflammation: Less prominent
  • Obliterative fibrosis of larger ducts: Characteristic feature
  • Periportal copper: Present
30
Q

Describe the main stages of Primary Biliary Cholangitis.

A
  • Autoimmune destruction of bile duct epithelium – dense lymphocytic infiltration and granulomas
  • Proliferation of small bile ducts (trying to re-generate)
  • Architectural disturbance within portal tracts portal and bridging fibrosis, which may lead to:
  • Cirrhosis
31
Q

Identify the main symptoms of primary biliary cholangitis.

A

Jaundice, pruritis, xanthelasmata (because TGs not processed properly in liver), itch

32
Q

Describe the levels of liver enzymes in primary biliary cholangitis.

A

• Raised ALP + IgM, AMA

33
Q

Define primary biliary cholangitis.

A

“Autoimmune disease of the liver. It results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver, a condition called cholestasis. Further slow damage to the liver tissue can lead to scarring, fibrosis, and eventually cirrhosis.”

34
Q

Define primary sclerosing cholangitis.

A

“Idiopathic chronic hepatobiliary disease characterized by diffuse inflammation and fibrosis of the extrahepatic biliary system resulting in patchy, irregular stricturing of the bile ducts. Progressive bile duct obliteration to cirrhosis, hepatic failure, and bile duct cancer”

35
Q

Define Haemochromatosis. Is this a primary or secondary process ?

A

Iron deposition in the liver causing alteration of architecture → fibrosis → cirrhosis

Can be primary (caused by autosomal recessive alteration of HFE gene which means we cannot process iron adequately in liver)
Can be secondary (e.g. haematology patient with bone marrow fibrosis, and need repeated transfusions, each of which has a lot of iron which leads to accumulation of Iron)

36
Q

Describe the treatment for Haemochromatosis.

A

Regular venesection + test iron and ferritin levels (to check treatment is working, those levels should decrease over time)

37
Q

Briefly describe the causes, and effects of α-1-antitrypsin Deficieny disease.

A

Autosomal recessive disorder associated with low levels of α-1-antitrypsin in the bloodstream (normally stops enzymes breaking down ourselves), either because abnormal α-1-antitrypsin, or because liver unable to secrete α-1-antitrypsin.
Resulting in proteins build up in hepatocytes as hyaline (can lead to cirrhosis, and in general associated with emphysema).

38
Q

Briefly describe the causes, and effects of Wilson’s disease.

A

• Autosomal recessive disorder

• Failure of the liver to excrete copper in bile, resulting in:
→ (Primary) build up of copper in liver → cirrhosis
→ build up of copper in brain tissue → neurological dysfunction
→ build up of copper in iris of eye → Kayser-Fleischer rings

39
Q

Identify the test for Wilson’s disease.

A

Caeruloplasmin (copper-binding protein) in the blood (low)

40
Q

Identify the main liver tumours.

A

Developmental/Hamartomas (i.e. started at/before birth, then stopped growing when you stopped)
• Cysts
• Hamartomas

Benign (often incidental findings)
• Adenoma, haemangioma
• Liver cysts

Malignant
• Metastases (most common malignant tumour of liver, most commonly from colon)
• Primary:
- Hepatocellular carcinoma (cirrhosis makes you more likely to get it)
- Cholangiocarcinoma

41
Q

Describe the structure, and aetiology of hepatocellular carcinoma.

A 
• Often multifocal 
• Aetiology: 
-Cirrhosis (any cause of cirrhosis) 
-Aflatoxins – fungal origin
-Hepatitis B + C viruses
42
Q

Identify pathologies of the biliary system.

A 
• Congenital malformations 
– Atresia (no patent common bile duct)
– Choledocal cysts
• Gallstones (cholelithiasis) 
• Cholecystitis (if block gall bladder)
• Cholangiocarcinoma
• Obstruction in the biliary tree (can be caused by any of the above)
43
Q

Cholangiocarcinoma

  • Tumor of ?
  • Associated diseases
  • Symptoms
  • Complications
A

Cholangiocarcinoma

  • Arises from bile duct epithelium anywhere in the biliary system (intra- and extra-hepatic)
  • Associated diseases: UC. Also, higher risk of cholangiocarcinoma if primary sclerosing cholangitis
  • Symptoms: Obstructive jaundice, itch, weight loss and lethargy
  • Complications: (often present late so) can lead to rupture of common bile duct or gallbladder – prognosis poor
44
Q

What are the main risk factors for gall stones ?

A
  • Female, fair, fat, forty, fertile

* Diabetes mellitus

45
Q

What are gall stones made of ?

A

• Cholesterol, bile pigment or mixed (commonest)

46
Q

What are possible complications/effets of gall stones ?

A

• Can cause cholecystitis (if blocks neck of gall bladder), obstructive jaundice (If block common bile duct, resulting in ascending infection and cholangitis), pancreatitis (if blocks pancreatic duct at outflow), cholangiocarcinoma (because irritate lining of biliary epithelium with gall stones)

47
Q

Where, besides the gall bladder, can gall stones form ?

A

Can form in bile ducts within liver

48
Q

Define Cholecystitis. What is its pathogenesis ?

A

Painful inflammation of the gallbladder’s wall.

ACUTE
• Usually caused by gallstones
• Initially sterile then becomes infected
• May lead to abscess/rupture

CHRONIC
• Invariably related to gallstones
• Chronic inflammation with wall thickening

49
Q

What are the symptoms of acute, and chronic cholecystitis ?

A 
ACUTE
RUQ pain (biliary colic, especially after a fatty meal), fever, nausea/vomiting

CHRONIC
Don’t generally present (see them much further down on the line usually)

50
Q

Identify a congenital problem which affects the pancreas.

A

Annular Pancreas, part of pancreas rotates the wrong way, round the second part of the duodenum and therefore squeezes it.

51
Q

What are the main consequences of annular pancreas ?

A

Causes obstruction – polyhydramnios (since intrauterine fetus cannot process amniotic fluid, leading to build up of amniotic fluid) which leads to low birth weight. Also poor feeding

52
Q

What are the main consequences of acute pancreatitis ?

A

• Causes catastrophic metabolic consequences –
↓ calcium, ↓ albumin, ↑ glucose (because pancreas inflamed so not producing any insulin)

  • Massive fluid losses (into retroperitoneal space due to inflammation and loss of albumin) → SHOCK
  • High mortality rates
53
Q

What is a diagnostic sign of acute pancreatitis ?

A

• High serum amylase is diagnostic of acute pancreatitis

54
Q

Identify the main causes of acute pancreatitis.

A
  • Shock
  • Alcohol
  • Trauma to pancreas
  • Mumps virus
  • Gallstones
  • Hypothermia
  • Scorpion poison
55
Q

Describe the pathogenesis of chronic pancreatitis.

A

Chronic pancreatitis occurs as a result of multiple episodes of of acute pancreatitis.

56
Q

What are the main effects of chronic pancreatitis ?

A

• Causes fibrosis of pancreas (and therefore loss of function of pancreas) – may lead to
diabetes mellitus
• Reduced production of enzymes

57
Q

Identify the treatment necessary for the reduced production of enzymes which occurs in chronic pancreatitis.

A

Creon (supplements)

58
Q

PANCREATIC CARCINOMA

  • Type of tumour
  • Risk factors
  • Symptoms
  • Prognosis
  • Management
A

PANCREATIC CARCINOMA

  • Type of tumour: Adenocarcinoma
  • Risk factors: Associated with smoking and diabetes mellitus
  • Symptoms: Presents with painless, progressive jaundice (painless because blocks common bile duct from outside) + weight loss (but silent until advanced)
  • Prognosis: Poor
  • Management: May be operable if small and close to ampulla

MD3002 (95 decks)

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