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Disease of hepatobiliary system > CP 59 - Disease of Hepatobiliary & liver tumours and billary > Flashcards

CP 59 - Disease of Hepatobiliary & liver tumours and billary Flashcards

1
Q

when will jaundice be visible to human eyes

A

when bilirubin >40 umol/l

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2
Q

what is pre-hepatic jaundice?

A

due to too much bilirubin produced - haemolytic anaemia

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3
Q

what is hepatic jaundice

A

due to too few functioning liver cells - acute diffuse liver cell injury, end stage chronic liver disease, inborn errors

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4
Q

what is post-hepatic jaundice

A

bile duct obstruction - stone, stricture, tumours of bile duct, pancreas

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5
Q

what is bilirubin?

A

broken down product of haemoglobin

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6
Q

how is bilirubin excreted out of the body

A

by hepatocyst through converting unconjugated bilirubin into conjugated bilirubin which is soluble in water and excreted in bile

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7
Q

what happens to conjugated bilirubin if bile duct is blocked

A

reabsorb by hepatocyst and excrete in urine instead

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8
Q

what happen to bilirubin once it passes into the intestine

A

it will be converted into by bacteria to faecal urobilinogen and makes up the brown colour of faeces

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9
Q

where is erythrocytes engulf and digested

A

in spleen by splenic macrophages

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10
Q

what is the explanation of pathogenesis for pre-hepatic jaundice?

A

unconjugated - then bound to albumin which is insoluble and so not excreted - ie yellow colour only

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11
Q

what is the explanation of pathogenesis for hepatic jaundice?

A

bilirubin mainly conjugated and so soluble - yellow colour and dark urine

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12
Q

what is the explanation of pathogenesis for post- hepatic jaundice?

A

bilirubin is conjugated and so soluble and excreted just can not get to the gut - yellow eyes, pale stool and dark urine

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13
Q

what are some examples of liver enzymes which can be used for testing for liver disease

A

liver enzymes -

Leak from hepatocytes – ALT, AST, (mild increase - chronic liver disease, v. high acute liver disease)

Leak from bile ducts – Alk phos (high in obstructive jaundice and chronic biliary disease)

bilirubin, albumin, clotting factors

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14
Q

what is the most important pathological features in liver with obstructive jaundice

A

bile in liver parenchyma

increase in time - portal tract expansion, oedema of the liver, accumulation of bile salts and copper (bile salts in skin - patients itchy)parenchyma

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15
Q

what is the most important histopathological features in liver with obstructive jaundice

A

bile plug in canaliculae between hepatocytes

Ductular reaction –
Portal tract enlarged by increase
In ductules and
oedematous fibrous tissue

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16
Q

how can suspected jaundice be investigated

A

USS for dilated ducts in obstruction - biopsy if nto dilated duct

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17
Q

what is the commonest cause to non-obstructive jaundice?

A

acute hepatitis

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18
Q

how long does chronic hepatitis has to be in order for it to be chronic?

A

over 6 months

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19
Q

causes of acute hepatitis

A

acute

  • inflammatory - viral, drugs, autoimmune
  • toxic/metabolic injury - alcohol, drugs etc
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20
Q

what are some of the presentation of acute hepatitis?

A

vary within a spectrum - Asymptomatic, malaise, jaundice, coagulopathy, encephalopathy, death

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21
Q

what are some of the histological changes i acute hepatitis?

A

Mild

apoptotic hepatocytes - acidophil body - spotty necrosis

presence of inflammatory cells

overall - lobular disarray

Severe

all hepatocytes have died - confluent panacinar necrosis

intermediate severe

bridging necrosis

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22
Q

what are the causes of chronic hepatitis

A

-Immunological injury –

virus, autoimmune, drugs

Toxic/metabolic injury – fatty liver disease, alcohol, non-alcoholic fatty liver disease (NAFLD), drugs

Genetic inborn errors – iron, copper, alpha1antitrypsin

Biliary disease – autoimmune, duct obstruction, drugs,

Vascular disease – clotting disorders, drugs

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23
Q

how does chronic liver disease process?

A

During any chronic liver disease,
scarring gradually increases and starts to link vascular structures (bridging)
eventually transforming the liver tissue into separate nodules – end stage = cirrhosis.

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24
Q

what cause Hep A?

A

Picorna RNA

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25
what cause Hep B?
Hepadna DNA
26
Wha cause Hep C
Flavivirus RNA
27
what other virus can also cause hepatitis?
EBV, CMV, HSV - usually in immunocompromised host
28
what are the different degrees of changes in the liver due to alcohol consumption?
fatty changes, alcoholic steatohepatitis, cirrhosis
29
what is the fatty changes due to alcohol consumption in the liver?
steatosis
30
what is the histological features of alcoholic steatohepatitis?
steatosis, Ballooned hepatocyte with Mallory Body, inflammatory cells progress to fibrosis in portal tracts and around hepatocytes (pericellular fibrosis)
31
what does NAFLD stands for?
non-alcoholic fatty liver disease
32
what can NAFLD leads to
Steatosis, steatohepatitis, cirrhosis, HepatoCellular Carcinoma
33
what is associated with NAFLD?
Metabolic syndrome – obesity, type 2 diabetes, hyperlipidaemia, also some drugs
34
what are some examples of drug induced liver injury
paracetamol
35
what does DILI stands for?
drug induced liver injury
36
what can paracetamol do to the liver?
acute liver failure as paracetamol is toxic and cause intrinsic hepatotoxicity
37
what does paracetamol cause in the liver histologically
uniform zonal necrosis - high proportion of hepatocytes in a predictable, zonal distribution, without any inflammation.
38
what is the mechanism of paracetamol toxicity
if safe dosage - then metabolism by 2 safe pathways excess - metabolise by P45o to a toxic metabolite and bind to the membrane of hepatocytes and cause necrosis
39
what is the treatment for paracetamol
N-acetyl cystein (restore Glutathione)
40
Definition of cirrhosis?
defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.
41
what can cause cirrhosis?
end point for chronic liver disease prolonged ``` alcohol Non-alcoholic steatohepatitis Chronic viral hepatitis – B, C Autoimmune liver disease Metabolic - alpha 1 antitrypsin, iron, copper ```
42
macroscopically what is the liver turned into in cirrhosis?
a mass of regenerating nodules wrapped by fibrosis scar tissue
43
what are some complication of cirrhosis?
structural changes - fibrosis - Portal hypertension, portal vein hypertension, increased blood flow, oesophageal varices Liver cell failure – unable to maintain homeostasis - Synthetic - oedema, bruising, muscle wasting Detoxifying – drugs, hormones, encephalopathy, Ascites – low albumin, portal hypertension, hormone fluid retention (aldosterone) excretion - jaundice, itchy hepatocellular carcinoma
44
what is Alpha 1 antitrypsin deficiency
Alpha 1 antitrypsin is a protein made in the liver excreted into blood where it functions to neutralise proteolytic enzymes, particularly from active polymorphs - inborn error Abnormal anti-protease which cannot be exported from hepatocyte Accumulates in liver cells and injures them – cirrhosis Insufficient in blood, failure to inactivate neutrophil enzymes
45
what is haemochromatosis
Inborn error of iron metabolism - ‘bronzed diabetes’ ``` iron accumulate in Liver - cirrhosis Pancreas - diabetes Skin - pigmented Joints – arthritis heart - cardiomyopathy ```
46
what is wilson's disease
inborn error of copper metabolism copper accumulate in liver – cirrhosis Eyes – Kayser-Fleischer rings – brown ring around the eye Brain – ataxia, etc.
47
what are the systemic effects of liver failure
``` Ascites Muscle wasting Bruising Gynaecomastia Spider naevi ```
48
definition of portal hypertension
Increased pressure of blood in the portal veins (
49
what is the major risk factor for hepatocellular carcinoma?
cirrhosis
50
what are the 4 reasons why you would die from cirrhosis?
ascite (an accumulation of fluid in the peritoneal cavity that exceeds 25 mL) , liver cell failure, infections and cancer
51
what are the risk factors for HCC?
male, obesity, alcohol, viral hepatitis (Hep B & C)
52
what are the macroscopic features of HCC?
Expansile soft nodules, often green (bile)
53
what are the microscopic features for HCC?
hepatocytes like, may produce bile - diagnostic (confirm with immunohistochemistry)
54
what are the treatment for HCC?
surgery - if non-cirrhotic transplant embolisation chemo & radio
55
what are some of the cancer which will metastasis to liver?
large bowel, lung, pancreas, breast, stomach, melanoma
56
what are cholangiocarcinoma?
Adenocarcinoma arising in the bile ducts
57
what does bile contain?
bile salts, phospholipids, cholesterol, bilirubin and calcium salts, + mucin from peribiliary gland
58
what is gallstones
concentration of bile precipates
59
what are the different types of gallstones
cholesterol stones - yellow, opalescent, pigment stones - small black in haemolytic anaemia mixed stones (most common) contain calcium
60
what are some of the complication of gallstones ?
inflammation of the gallbladder (cholecystitis) predisposition to carcinoma of the gallbladder obstruction of the biliary system resulting in biliary colic (pain when gall stone block the bile duct) and jaundice infection of static bile, causing cholangitis and liver abscesses pancreatitis
61
what can cause acute cholecystitis?
duct blocked by stone, Initially sterile, later infected. Large, swollen, congested, ulcerated.
62
what are some complications for acute cholecystitis?
empyema (pus in peritoneal space), rupture
63
what can cause chronic cholecystitis?
usually gallstone
64
what can chronic cholecystitis cause?
fibrosis and inflammation and can cause Rokitansky-Aschoff sinus

Disease of hepatobiliary system (4 decks)

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