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Y3 IWB > PATHOLOGY- Hepatobiliary disorders > Flashcards

PATHOLOGY- Hepatobiliary disorders Flashcards

1
Q

Where is the liver located in the body

A

Upper right quadrant of abdominal cavity

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2
Q

How much does the liver weigh in adults

A

Around 1.5kg

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3
Q

What is a different about the liver

A

It has a dual blood supply

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4
Q

Describe the livers dual blood supply

A
  1. The intestines/spleen supplies blood through to the portal vein (70%)
  2. The aorta supplies blood through the coelia axis into the hepatic arteries (30%)
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5
Q

Why does the liver get most of its blood from the intestines

A

Organisation important - processing of materials / pathogens from gut before they enter into systemic circulation.

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6
Q

What is the most of the liver made up of and how are these arranged

A

hepatocytes, arranges in rows, cords or ‘plates’

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7
Q

What structures can you see on the liver microscopically

A

Portal tracts
Hepatic veins
Bile ducts

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8
Q

What is the role of the portal tracts

A

Supplies blood from the portal vein and hepatic arteries, allowing it to travel down the sinusoids (gaps) between the chords of hepatocytes

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9
Q

What is the role of the hepatic veins

A

Where blood exits the liver

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10
Q

What is the role of bile ducts

A

Allows bile produced by the liver cells to exit through the portal tract, against the flow of blood

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11
Q

what is the role of the liver

A

Protein metabolism
Nitrogen excretion
Carbohydrate metabolism
Lipid metabolism
Bile production/metabolism
Bilirubin metabolism
Hormone/drug inactivation
Immunological functions

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12
Q

Why is protein metabolism important in the liver

A

Mostly all circulating proteins made in liver e.g. clotting factors, albumin eti
Serious manifestation of liver failure e.g. impaired clotting, dec in albumin, resulting in oedema/ ascities

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13
Q

How does the liver excrete nitrogen

A

Amino acids are broke down in to ammonia and excreted through urine

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14
Q

What is carbohydrate metabolism needed in the liver

A

Glucose homeostasis
Blood sugar regulation

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15
Q

why is bile production/metabolism important ion the liver

A

For digestion/absorption of lipids

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16
Q

What is bilirubin metabolism in the liver and what is the effect of impaired excretion

A

Breakdown product of RBC
Jaundice

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17
Q

What are the 2 immunological functions of the liver

A

Acts a sieve for bacteria that are passed from the GI tract through the portal vein
80-90% of innate immune proteins made in liver

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18
Q

What is bilirubin

A

A product of RBC/harm breakdown

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19
Q

What is the initial issue with bilirubin

A

Not water soluble

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20
Q

How does bilirubin travel around the body

A

Albumin (bilirubin is a protein-bound molecule)

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21
Q

What is bilirubin known as when it is bound to albumin

A

Unconjugated bilirubin

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22
Q

When happens when unconjugated bilirubin passes through the liver

A

Becomes conjugated and water soluble

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23
Q

what is the water soluble bilirubin known as

A

Conjugated bilirubin

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24
Q

What happens to bilirubin once it has become conjugated and water soluble

A

Conjugated bilirubin is excreted in the bile (produced by liver cells), passes it out into the biliary tree through the bile ducts, into the gut

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25
Q

what happens to conjugated bilirubin in the gut

A

It is converted to urobilinogen/stercobilinogen
Most passes out in faces as stercobilin
Some absorbed back into the blood

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26
Q

Why is faeces brown

A

Due to stercobilin

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27
Q

what happens to conjugated bilirubin that is absorbed back in to the blood

A

Either enters enterohepatic circulation or excreted in urine

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28
Q

What is the most common sign of liver disease

A

Jaundice

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29
Q

when does jaundice occur

A

Increased bilirubin

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30
Q

when is jaundice visible

A

When bilirubin >40umol/l

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31
Q

What are the 3 types of jaundice

A

Pre-hepatic = too much bilirubin produced
Hepatic = too few functioning liver cells
Post-hepatic = bile duct obstruction

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32
Q

When would you see pre-haptic jaundice

A

Haemolytic anaemia

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33
Q

When would you see hepatic jaundice

A
  • Acute diffuse liver cell injury
  • End stage chronic liver disease
  • Inborn metabolic errors
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34
Q

When would you see post-hepatic jaundice

A

Stone, stricture, tumour- bile duct, pancreas

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35
Q

What are some markers of liver cell damage

A
  • Liver enzymes ALT and AST leakage from damaged hepatocytes
  • Liver enzyme ALP leakage from damaged bile duct cells
  • Albumin
  • Clotting
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36
Q

Name 2 enzymes that leak from damaged hepatocytes in liver disease, acting as markers for liver disease

A
  • ALT - Alanine aminotransferase
  • AST - Aspartate aminotransferase
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37
Q

What does it mean if there is mild slow progressive increase of damaged hepatocytes causing leakage

A

chronic liver disease

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38
Q

What does it mean if there is sudden massive increase of damaged hepatocytes causing leakage

A

Severe acute liver disease

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39
Q

Name an enzyme that leaks from damaged bile duct cells in liver disease, acting as markers for liver disease

A

ALP - Alkaline Phosphatase

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40
Q

Why does low albumin indicate chronic liver disease

A

As it is synthesised by the liver and usually has a long half life

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41
Q

Why does low clotting factors indicate acute or chronic liver disease

A

Clotting factors produced by liver
Have a short half life
CF used to test whether blood is clotting properly, if not then LD

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42
Q

How would you investigate if someone has jaundice

A

Ultra-sound scan to check for dilated bile ducts

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43
Q

If you did an ultrasound scan on somebody with jaundice and there bile ducts were dilated, what does this indicate

A

Obstruction of bile ducts

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44
Q

If you did an ultrasound scan on somebody with jaundice and there bile ducts were not dilated, what would you do next and why

A

Biopsy of liver
To visualise the abnormality within the liver

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45
Q

Most non obstructive cases of liver disease are due to what

A

Hepatitis

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46
Q

What is hepatitis

A

Inflammation of the liver/damage to the liver that isn’t Neoplastic

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47
Q

What are the causes of acute and chronic hepatitis

A
  • Viral
  • Alcohol / obesity
  • Drugs
  • Inherited disorders:
    • Haemochromatosis (iron)
    • Wilson’s disease (copper)
    • Alpha-1-antrypsin deficiency
  • Autoimmune
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48
Q

What is hepatitis clinically/biochemically defined by

A

Raised liver enzymes (ALT/AST)
Indicates damage

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49
Q

What is acute hepatitis
How long does it last
What are the signs
How is it detected

A
  • Acute sudden liver injury, caused by something that goes away
  • Short-lived, resolves
  • No signs (unless severe)
  • Incidentally at blood tests
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50
Q

What is chronic hepatitis
How does it differ to acute
What does it cause

A
  • Anything causing persistent liver injury (i.e. doesn’t go away)
  • Persistent cycle of damage and repair
  • Long term liver damage
51
Q

What are symptoms of acute hepatitis from common to rare

A

Asymptomatic
Malaise
Jaundice
Coagulopathy
Encephalopathy
Death

52
Q

What 2 things does the severity of acute hepatitis depend on

A
  1. How many hepatocytes are damaged as a result of the hepatitis
  2. How well the liver is able to regenerate the lost cells
53
Q

What are the causes of acute hepatitis

A

Anything that causes short term liver cell injury
E.g.
Viral
Drugs
Autoimmune
Toxic/metabolic injury (alcohol/paracetamol overdose)

54
Q

What is chronic hepatitis

A

chronic liver disease in which the damaging agent is persistent (doesn’t go away)

55
Q

What can chronic hepatitis progress to

A

Cirrhosis- but may be partially reversible

56
Q

what are the causes if chronic hepatitis

A
  • Immunological - viral, autoimmune, drugs
  • Toxic / metabolic - “fatty liver disease” - alcohol, non-alcoholic fatty liver disease (NAFLD)
  • Genetic - iron, copper, alpha-1-antitrypsin
57
Q

How does chronic hepatitis cause damage to the liver

A
  1. Damage begins and is concentrated around portal tracts
  2. The cycle of hepatocytes injury and repair causes scarring
  3. This gradually increases and starts to link vascular structures (the PTs and CVs) by scar tissue
  4. This is bridging fibrosis
  5. Eventually transforming the liver tissue into separate nodules
  6. At the end stage this results in cirrhosis
58
Q

What are the causes of chronic liver disease

A

Viral hepatitis

59
Q

List the hepatrophic (liver specific) viruses that cause viral hepatitis

A
  • A,B and C
  • D (hepatitis delta virus)
  • E
60
Q

Hepatitis D is found in who

A

Only in people with hep b

61
Q

what is hepatitis E

A

recently discovered, fairly common, faecal-oral transmission mainly via contaminated water, mild self-limiting if healthy

62
Q

List other viruses that cause hepatitis as part of systemic disease

A

EBV
CMV
HSV

63
Q

What characteristic effect does excessive alcohol intake have on the liver

A
  • fatty change
  • alcohol steatohepatitis
  • cirrhosis
64
Q

What does alcohol liver injury depend on

A

Dose (intake)
Susceptibility

65
Q

What is indicated if there are characteristic features such as fat chnage to the liver in the absence of alcohol

A

Non-alcoholic fatty liver disease
NAFLD

66
Q

What do you see microscopically with liver damage caused by alcohol

A

Fatty change (steatosis)
Ballooned hepatocyte with Mallory body
Inflammatory cells

67
Q

What is now regarded as the most common cause of liver disease

A

NAFLD

68
Q

What changes can be seen microscopically with NAFLD

A

Same as alcoholic liver disease
- Steatosis (fatty change), steatohepatitis, cirrhosis, HCC

69
Q

Why can NAFLD result in liver injury

A

Excessive fat accumulation

70
Q

What is NAFLD associated with

A

metabolic syndrome (obesity, diabetes, hyperlipdaemia etc).

71
Q

What is the treatment for NAFLD

A

Address the metabolic syndrome (causes)

72
Q

What is statohepatitis

A

Fatty change plus hepatocyte injury

73
Q

Hepatotoxicity can be either what 2 things

A

Intrinsic
Idiosyncratic

74
Q

What can hepatotoxic drugs lead to

A

Drug induced liver injury (DILI)

75
Q

what is intrinsic hepatotoxicity

A
  • drug that causes everyone liver injury if excessive dose is administered
  • Susceptibility will vary but liver injury is entirely predictable
  • e.g. paracetamol.
76
Q

What is idiosyncratic hepatotoxicity

A
  • Liver injury is rare and unpredictable
  • e.g. antibiotics - small numbers of individuals
  • Mechanism - metabolic and immunologic response variability
    • Production of rare drug metabolites +/- exaggerated immune response
77
Q

Generally drugs cause..

A

Acute liver injury

78
Q

What is the most common symptom for DILI

A

Jaundice

79
Q

Which type of drugs can cause liver injury

A

Any drug
Same drug can cause different pattern of injury in different patients
Time of onset is variable

80
Q

When does DILI usually improve and what is prevented

A

Stopping drug
Chronic liver disease but not always

81
Q

What are the effects of paracetamol overdose

A

sudden (2-3 days) massive hepatocellular necrosis (pale areas)
No inflammation

82
Q

Which part of the liver is affected by paracetamol overdose

A

Mainly around central veins

83
Q

What can happen if there is no urgent transplant with paracetamol overdose

A

Death

84
Q

Give 2 examples of an inherited liver disorder

A

Haemochromatosis
Wilsons disease
Alpha 1 antitrypsin deficiency

85
Q

What is haemochromatosis

A

Inherited disorder of iron metabolism (HFE gene) causing increased iron absorption from the gut

86
Q

what effect does haemochromatosis have on the liver

A

Iron accumulation in the liver, causing chronic liver injury and eventually cirrhosis

87
Q

what is Wilson’s disease

A

Impaired excretion of copper causes accumulation in liver resulting in chronic liver injury/cirrhosis

88
Q

What effect does alpha 1 antitrypsin deficiency have on the liver

A

Alpha 1 antitrypsin can’t be excreted and accumulate in the liver causing chronic liver injury, resulting in cirrhosis (and emphysema in lungs)

89
Q

What are autoimmune liver diseases

A

Disturbance of normal immune regulation leading to recognition of self-antigens

90
Q

How can autoimmune liver diseases manifest

A

Can manifest with either autoimmune mediated destruction of hepatocytes (autoimmune hepatitis)
OR
Autoimmune mediated damage to bile ducts (autoimmune biliary diseases primary sclerosing cholangitis / primary biliary cirrhosis)

91
Q

Who is autoimmune hepatitis more common in

A

Women

92
Q

What can autoimmune hepatitis present as

A

Acute or chronic hepatitis

93
Q

How do you diagnose autoimmune hepatitis

A
  • Autoantibodies e.g. anti-nuclear, smooth muscle, etc
  • Raised IgG, ALT
  • Assoc. autoimmune diseases
94
Q

What would you see in a liver biopsy in someone with autoimmune hepatitis

A
  • Interface hepatitis
  • Lots of plasma cells
95
Q

What is the treatment for autoimmune hepatitis

A

Immunosuppression

96
Q

Why is it important to treat autoimmune hepatitis

A

To avoid progression to cirrhosis

97
Q

Name 2 biliary diseases (autoimmune liver diseases)

A

Primary biliary cholangitis
Primary sclerosing cholangitis

98
Q

What is seen in primary biliary cholangitis diagnosis

A

Anti-mitochondrial antibodies
Inc IgM
Inc ALP (bile duct damage)
Bile duct granulomas

99
Q

What can primary biliary cholangitis progress to

A

Cirrhosis

100
Q

What is primary sclerosing cholangitis associated with

A

Ulcerative colitis

101
Q

How is primary sclerosing cholangitis diagnosed

A

pANCA antibodies but diagnosis is via imaging

102
Q

What characteristic changes are there in primary sclerosing cholangitis

A

Periductal onion skin fibrosis around bile ducts

103
Q

what can primary sclerosing cholangitis progress to

A

Cirrhosis

104
Q

What is cirrhosis

A

Diffuse change in the liver structure due to chronic liver disease.
* Development of fibrous septa that subdivide the parenchyma into nodules as a result of bridging
fibrosis.

105
Q

Cirrhosis isn’t a specific disease but

A

A general end point go ALL progressive chronic liver diseases

106
Q

how long does cirrhosis take to develop

A

Slow to develop, decades

107
Q

Cirrhosis is clinically silent until when

A

The liver function fails (decompensation) leading to signs of liver failure/portal hypertension

108
Q

What ate the 2 components of cirrhosis

A

Regenerative nodules go hepatocytes
Surrounded by sheets/bands of fibrous tissue

109
Q

What is the cause of cirrhosis

A

Liver disease that wont go away i.e. chronic liver disease

110
Q

What are the potential complications with cirrhosis

A
  • Liver failure
  • Portal hypertension
  • Infection
  • Hepatocellular carcinoma
111
Q

What can you develop with sudden severe liver damage

A

Acute liver failure e.g. paracetamol OD

112
Q

Why may someone have cirrhosis and be unaware of it

A

Some residual function left
If original disease is removed and there’s cirrhosis, can still show no abnormality on liver function test

113
Q

Is the liver is unable to maintain its normal function what can occur

A

Decompensated liver disease leading to liver failure

114
Q

List features relating to impaired liver synthetic/metabolic function

A
  • Hypoalbuminemia / clotting factor deficiencies - bruising / bleeding
  • Ascites - due to dec in albumin & aldosterone disturbances
  • Encephalopathy - due to impaired breakdown of nitrogenous substances (mimic NTs)
  • Gynaecomastia - due to impaired estrogen breakdown
115
Q

What is portal hypertension

A
  • Structural abnormalitv in liver (cirrhosis)
  • Impairs blood flow - back pressure in portal vein
116
Q

What are the causes of portal hypertension

A
  • Ascites (combination of liver failure and pressure effects)
  • Splenomegaly (due to back pressure on spleen)
117
Q

Why do porto-systemic shunts occur in portal hypertension

A

Blood by-passes liver due to increased resistance to blood flow

118
Q

What effects do porto-systemic shunts have

A
  • Oesophageal varices, haemorrhoids, “caput medusae”
  • Peri-splenic varices
  • Prone to bleeding / rupture BUT also BYPASSES functional liver
119
Q

How does infection cause cirrhosis

A
  • Cells within the liver (Kuppfer cells)
  • Act to fight infection
  • Impaired function / bypass -> † infection risk
120
Q

What is hepatocellular carcinoma

A

Malignant tumour of hepatocytes

121
Q

List benign liver tumours

A

haemangioma, bile duct adenoma, FNH, HA

122
Q

List malignant liver tumours

A

cholangiocarcinoma, metastatic tumours(CRC)

123
Q

What are some possible complications with liver disease in regard to dental tx

A
  • Coagulopathies, drug-toxicity (dec in metabolism)
  • Infection (hepatitis)
124
Q

If in doubt when treating someone with liver disease, who should u consult

A

BNF

Y3 IWB (31 decks)

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