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BDS2; FHHD > SP4: Liver Diseases > Flashcards

SP4: Liver Diseases Flashcards

1
Q

Describe the anatomy of the liver

A
  • 2 main lobes
  • separated by flaciform ligament
  • 8 segments based on branches of blood supply
  • hepatic artery = oxygenated blood
  • hepatic portal vein = nutrients from small colon
  • gallbladder connects to common hepatic duct via cystic duct
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2
Q

What caries bile from the liver to duodenum

A

It is produced in the gallbladder, carried in the cystic duct to the common hepatic duct which carries the bile to the duodenum

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3
Q

Describe liver histology

A
  • tissue is made of hepatocytes
  • sheets of hepatocytes are separated by sinusoids (where the blood vessels will travel through)
  • hepatic tissue is arranged into lobules = functional units
  • central vein is located at the centre of each lobule
  • portal tract is present at each corner of a lobule (contains hepatic artery, portal vein and bile duct)
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4
Q

What are acini

A

They are located between two central veins (centre of one lobule to another) - this is divided into 3 zones

Zone 1 = Closest to portal tract
Zone 3 =Closest to central vein

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5
Q

What are the functions of the liver

A

Detoxification and breakdown of toxins, hormones and drugs

Synthesis of : bile, protein, gluconeogenesis, cholesterol, triglycerides, RBCs in foetal liver, clotting factors

Storage of glucose (as glycogen), vitamins and minerals

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6
Q

What happens in response to liver damage

A
  1. Hepatocyte degeneration - so intracellular accumulation
  2. Hepatocyte necrosis and apoptosis
  3. Inflammation
  4. Regeneration
  5. Fibrosis and formation of scar tissue
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7
Q

What are the symptoms of liver damage

A
  • Jaundince (due to increased bilirubin giving yellowing)
  • Oedema (fluid retention in tissues)
  • Ascites (distension of abdomen)
  • Cerebral dysfunction (drowsiness and confusion)
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8
Q

Outline the process of bilirubin metabolism

A
  1. Hb released from RBCs
  2. Heme oxygenase converts heme to biliverdin
  3. Biliverdin reductase reduces this to unconjugated bilirubin
  4. This is converted to conjugated bilirubin
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9
Q

What is jaundice

A

Raised serum bilirubin with bilirubin deposition in tissues

This can be classified by site or type

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10
Q

What are the pre-hepatic causes of jaundice

A

This is jaundice before bilirubin reaches the liver and is caused by

  1. Haemolytic anaemia : RBCs in circulation breakdown releasing haemoglobin and so bilirubin
  2. Internal bleeding : blood escaped from blood vessels is broken down
  3. Ineffective erythropoiesis
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11
Q

What are the intra-hepatic causes of jaundice

A

This is jaundice when the bilirubin has reached the liver and is caused by

  1. Impaired conjugation of bilirubin and diffuse hepatocellular disease
  2. Impaired excretion: intrahepatic bile duct disease
  3. Reduced uptake
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12
Q

What are the post-hepatic causes of jaundice

A

This is jaundice after bilirubin has left the liver and is caused by

  1. Extrahepatic biliary obstruction
    - gallstones produced in gallbladder
    - pancreatic cancer that compresses biliary tree
    - extrahepatic biliary atresia : no lumen in biliary tree so bile cannot flow
    - biliary strictures : narrowing causing bilirubin to accumulate
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13
Q

What are the hepatic causes of oedema and ascites

A
  1. Portal hypertension : high blood pressure in portal venous system
  2. Hypoalbuminaemia : low level of albumin in circulation which would normally help retain fluid in circulation due to osmolality
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14
Q

Outline the mechanism of oedema and ascites

A
  • high intrasinusodial pressure
  • leakage from hepatic lymphatics
  • Na + and water retention
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15
Q

What are the effects of portal hypertension

A

Portal systemic venous shunts

  • oesophagus = varices
  • rectum = haemorrhoids
  • ant. abdominal wall (caput medusae)

Splenomegaly (congestive) = enlarged spleen

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16
Q

How is cerebral dysfunction caused

A

Increased ammonia production in liver injury disrupts the urea cycle and this affects neurotransmission in the brain and CNS causing the following symptoms

  • decreased consciousness
  • rigidity
  • hyper-reflexia
  • asterixis (resting hand tremour)
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17
Q

What is hepatitis

A

Inflammation of the liver following injury - can be acute/chronic

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18
Q

What are the causes of hepatitis

A
  1. Viral
  2. Alcohol
  3. Drugs/toxins
  4. Autoimmune
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19
Q

What is hepatitis A

A

liver infection caused by faecal-oral spread; not chronic

20
Q

What is hepatitis B

A

liver infection caused by parenteral spread (IV, sex)

this is chronic in 5-10% and so can progress to chronic hepatitis an hepatocellular carcinoma

21
Q

What is hepatitis C

A

liver infection caused by parenteral spread which is chronic in >50% and can progress to chronic hepaptitis and hepatocellular carcinoma

22
Q

What is delta hepatitis viris/ Hepatitis D

A

It is a defective RN virus which is infective if encapsulated by HBV

  • it results from co infection with hep B and results in fluminant disease (rapidly escalating)
  • it is a chronic progressive disease
23
Q

What is hepatitis E

A

Water bourne and non chronic

24
Q

What are the symptoms of acute hepatitis

A
  • mostly non-specific; nausea, voomiting, abdo pain
  • specifics; loss of apetite, dark urine, jaundice
  • small portion can progress to acute liver failure
25
Q

Describe the pathological features of acute hepatitis

A

Macro = mild hepatomegaly (enlargement) and congestion

Micro;

  • scattered foci of lobular necrosis and inflammation
  • apoptotic bodies (of hepatocytes) = Councilman body
  • hepatocyte ballooning an necrosis
  • disruption of architecture causing lobular structure
  • inflammation of portal tracts thus many inflammatory cells
26
Q

What is a councilman body

A

Present in acute hepatitis where there are hepatocytes undergoing apoptosis and these are eosinophilic with irregular nuclei

27
Q

What is chronic hepatitis

A

Necroinflammatory disease in which hepatocytes are the target of attack caused by

  1. Hep B / B + D
  2. Hep C
  3. Autoimmune hepatitis
  4. Drug-induced hepatits
28
Q

What three histological changes occur in chronic hepatitis

A
  1. Inflammation (predominantly lymphocytic)
    - portal tracts
    - periportal interface hepatitis (piecemeal necrosis within lobular boundaries)
    - lobular
  2. Hepatocyte necrosis
    - bridging necrosis = portal to central/ portal to portal
    - confluent necrosis = larger area
  3. Fibrosis
    - portal/ periportal/ bridging and eventually cirrhosis
29
Q

What is cirrhosis and what histological changes can be seen

A

Irreversible and end stage liver disease

  • diffuse process
  • fibrous nodules (regenerative hepatocytes surrounded by fibrosis)
  • disruption of vascular architecture and blood flow
30
Q

What complications can arise with cirrhosis

A
  1. Portal hypertension

2. Hepatic failure

31
Q

What are the causes of cirrhosis

A
  • alcohol
  • viral hepatitis (B,C,D)
  • autoimmune hepatitis
  • primary and secondary biliary cirrhosis (damaged biliary tree)
  • metabolic causes
  • drugs
  • ideopathic thus not causal
  • venous outflow obstruction
32
Q

What are the metabolic causes of cirrhosis

A
  1. Haemochromatosis = impaired iron metabolism so there is iron acculimation within the tissue
  2. Wilson’s disease = defective copper metabolism so there is copper accumilation
  3. Alpha-1-antitrypsin deficiency = these proteins would normally protect the liver and lung from injury but they are insufficient
33
Q

What are the complications of cirrhosis

A
  • hepatic failure
  • hepatic encephalopathy = cerebral dysfunction due to ammonia
  • oesophageal varicies
34
Q

What is hepatic encephalopathy

A

This is where cerebral dysfunction arises due to ammonia because the portal blood bypasses liver which can have toxic or metabolic effects on the brain meaning there is a decreased consciousness which can potentially lead to coma

35
Q

What are oesophageal varices

A

These are massive haemorrhages due to portal dynamic shunts - the abnormal vessel dilation increases the risk of bleeding and this manifests as haemorrhoids in the rectum

36
Q

Describe the cell pathology of cirrhosis

A
  • cannot make out hexagonal lobules

- there are large spaces between sheets of hepatocytes

37
Q

What are the 8 features of hepatic failure

A
  1. Jaundice (increased bilirubin as hepatocyte dysfunction)
  2. Hypoalbuminaemia (decreased synthesis of albumin)
  3. Coagulopathy (decreased clotting factor synthesis)
  4. Disseminated intravascular coagulation (muli clots form)
  5. Raised serum urea (as urea cycle disturbance)
  6. Hepatorenal syndrome (reduced renal blood flow)
  7. Gynaecomastia (liver cant break down oestrogen)
  8. Encephalopathy
38
Q

What happens in alcoholic steatosis

A
  • fatty change; red liver tissue becomes soft and yellow
  • fibrosis
  • if alcohol consumption isnt reduced it can cause alcoholic hepatitis
39
Q

What happens in alcoholic hepatitis

A
  • fatty change
  • fibrosis
  • hepatocyte necrosis
  • inflammation : inflammatory cells seen in biopsy
  • Mallory’s hyaline (protein deposition); iron deposition
40
Q

What is alcoholic cirrhosis

A

Irreversible tissue breakdown due to alcohol

41
Q

What are the four malignant primary liver tumours

A
  1. Hepatocellular carcinoma (most common)
  2. Cholangiocarcinoma (developed from biliary tree)
  3. Angiosarcoma (originates from blood vessels in liver tissue)
  4. Hepatoblastoma (mainly in children)
42
Q

What are the sources of secondary metastatic tumours in the liver and what is the morphology

A
  1. Carcinoma (GIT and breast)
  2. Melanoma (skin)

Causes hepatomegaly and multiple nodule formation

43
Q

Describe the aetiology of hepatocellular carcinoma

A
  • majority develop in a cirrhotic liver
  • hep B, C
  • haemochromatosis
  • aflatoxin from fungi
  • alcohol, age, gender
44
Q

What are the clinical features of hepatocellular carcinoma

A
  • abdo pain, weight loss, hepatomegaly
  • raised serum alpha-feto protein
  • metastasis occur late stage in the lungs
  • survival <6 months (poor prognosis)
  • death is due to cachexia (XS weightloss and muscle wasting), varices (rupture of portal shunts), encephalopathy
45
Q

Describe the pathology of hepatocellular carcinoma

A

Macroscopy

  1. Unifocal mass = yellow/white, soft, haemorrhage, necrotic
  2. Multifocal
  3. Diffusely infiltrative

Microscopy

  • well differentiated tumours resembling normal liver trabeculae (rows)
  • poorly differentiated tumours mimic metastases

BDS2; FHHD (26 decks)

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