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Liver Pathology Flashcards

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1
Q

What is Cirrhosis?

A

Chronic inflammation and ireversible necrosis of hepatic parenchyma, leading to fibrosis

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2
Q

What are the causes of cirrhosis?

A

Alcoholic liver disease

Non alcoholic fatty liver disease

Hepatitis, most commonly B and C

Haemochromatosis, Wilsons

Drugs

Autoimmune hepatitis

PBC

CF

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3
Q

What is the most common cause of liver disease in the developing world?

A

Non alcoholic fatty liver disease

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4
Q

How does cirrhosis present?

A

Jaundice

Hepatomegaly and splenomegaly

Spider naevi

Palmer erythema

Gynaecomastia

Ascites

Caput medusae

Bruising/purpura

RUQ pain

Dupuytren’s contracture

Oedema

Leukonychia

Clubbing

Pruritis/scratch marks

Fetor Hepaticus

Hepatic flap/flapping tremor

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5
Q

What investigations are used in cirrhosis diagnosis and monitoring?

A

LFTs

  • Often normal
  • Decreased albumin

FBC

  • Thrombocytopenia

U&Es

  • Deranged in hepatorenal syndrome

Coagulation

  • Increased PT

Transient Elastography/fibro scan

  • Measures ‘stiffness’ of liver and level of fibrosis
  • Retest patient every 2 years at risk of cirrhosis

US

  • corkscrew arteries

Liver biopsy, confirms diagnosis

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6
Q

What coagulation factors are affected in liver disease

A

Vitamin K and factors 2,7,9,10

(2+7=9 not 10)

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7
Q

What is the most sensitive lab test in chronic liver disease/cirrhosis?

A

Thrombocytopenia

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8
Q

What is the best marker for declining liver function?

A

Albumin and coagulation

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9
Q

What test is first line in non alcoholic fatty liver disease diagnosis?

A

Enhanced liver fibrosis (ELF) blood test

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10
Q

What do LFTs show in non alcoholic fatty liver disease?

A

ALT>AST

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11
Q

What antibodies are associated with autoimmune hepatitis?

A

ANA (anti-nuclear antibodies)

SMA (anti-smooth muscle antibodies)

LKM1 (anti liver/kidney microsomal type 1)

Soluble liver-kidney antigen

IgG

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12
Q

How is cirrhosis managed?

A

Aimed at the underlying cause and preventing complications

Nutritional support

  • High protein and low Na diet
  • Alcohol abstinence

Surveillance

  • US and AFP every 6 months for hepatocelluar carcinoma
  • Endoscopy every 3 years for varices
  • MELD score every 6 months

Vitamin K, to correct clotting

Ascites management

Portal hypertension and varices management

Encephalopathy management

Liver transplant consideration

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13
Q

What scoring system determines the severity of cirrhosis?

A

Child Pugh Score

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14
Q

What factors does the Child Pugh Score take into consideration?

A

Each factor is given a score of 1 2 or 3, so minimum is 5 and maximum is 15

Albumin

Bilirubin

INR

Ascites

Encephalopathy

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15
Q

What number of points gives a Child Pugh Score A?

A

Less than 7

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16
Q

What number of points gives a Child Pugh Score B?

A

7-9

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17
Q

What number of points gives a Child Pugh Score C?

A

More than 9

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18
Q

What is the MELD score?

A

Used every 6 months in patients with compensated cirrhosis, givinga percentage estimated 3 month mortality and helps guide referral for liver transplant

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19
Q

What factors does the MELD score take into consideration?

A

Bilirubin

Creatinine

INR

Na

Dialysis

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20
Q

Name complications of cirrhosis

A

Malnutrition

  • Hypoglycaemia

Hepatic encephalopathy

Ascites

Thiamine deficiency

  • Wernicke’s and Korsakoff

Coagulopathy

Hepatocellular Carcinoma

Sepsis/Impaired immune system

Hepatorenal Syndrome

Variceal haemorrhage

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21
Q

What is hepatic encephalopathy?

A

Neuropsychiatric syndrome caused by the accumulation of ammonia in the blood stream due to the livers decreased ability to detoxify ammonia

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22
Q

How is hepatic encephalopathy managed?

A

Laxatives/Lactulose

  • Promote expulsion of ammonia
  • Oral but given rectally if patient is too drowsy

Oral Rifaximin

  • Used in refractory disease and to prevent disease in patients with recurrent encephalopathy despite lactulose
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23
Q

Give precipitating factors of hepatic encephalopathy

A

Infection/peritonitis

GI bleed

Post transjugular intrahepatic portosystemic shunt

Constipation

Sedatives

Diuretics

Hypokalaemia

Renal failure

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24
Q

How is alcoholic ketoacidosis managed?

A

IV thiamina and 0.9% NaCl

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25
How can the causes of ascites be grouped?
Those with a serum-ascites albumin gradient (SAAG) \<11 g/L or a gradient \>11g/L (indicating portal hypotension)
26
What are the causes of SAAG \>11g/l?
Cirrhosis Acute liver failure Liver metastases RHF Constrictive pericarditis Budd-Chiari syndrome Portal vein thrombosis Myxoedema
27
What are the causes of SAAG \<11g/l?
Nephrotic syndrome Malignancy Bowel obstruction Post-operative lymphatic leak
28
How is ascites managed?
Decreased Na intake Aldosterone antagonists Paracentesis/ascitic tap * With albumin infusion to revent post-paracentesis circulatory dysfunction Consider TIPS or transplant in refractory ascites Prophylactic oral ciprofloxacin, if increased risk of spontaneous bacterial peritonitis
29
What are complications of ascites?
Spontaneous bacterial peritonitis Compression of IVC Hepatorenal syndrome Transudate pleural effusion
30
How does spontaneous bacterial peritonitis present?
**Should always be considered in patients with known cirrhosis and ascites** Fever Abdominal tenderness/pain Abdominal distention Vomiting Altered mental state Inflammatory markers
31
What organism typically causes spontaneous bacterial peritonitis?
E-coli, most commonly Klebsiella Staph aureus
32
How is spontaneous bacterial peritonitis managed?
Ascitic culture prior to giving antibiotics IV Cefotaxime
33
Describe the pathophysiology of varices
Portal hypotension leads to the formation of collateral circulations, occurring when portal pressure exceeds 12mmHg
34
What is the management of variceal haemorrhage?
Prophylactic propanolol Correct clotting * Vitamin K * Fresh frozen plasma Terlipressin * Vasoactive agent to slow bleeding Prophylactic antibiotics * Quinolones Endoscopic Variceal Band Ligation * Carried out at 2 weekly intervals until all varices are eradicated Sengstaken-Blakemore tube * If uncontrolled haemorrhage TIPSS * Last resort treatment
35
What is a Transjugular Intrahepatic Portosystemic Shunt (TIPS)?
Connection made between portal vein and hepatic vein
36
What is Hepatorenal syndrome?
Renal failure in the presence of severe liver disease where all other causes have been excluded which is fatal within a week unless liver transplant is performed
37
What is the difference between type 1 and 2 hepatorenal syndrome?
Type 1 occurs rapidly whereas type 2 is slow progression
38
What is liver failure?
Acute necrotizing hepatitis leading to cell destruction
39
What are the 3 liver failure classifications?
Hyperacute or fulminant liver failure Acute liver failure Subacute liver failure
40
What is hyperacute liver failure?
Encephalopathy develops within 1 week
41
What is acute liver failure?
Encephalopathy develops within 2-4 weeks
42
What is subacute liver failure?
Encephalopathy develops within 4-8 weeks
43
What is the best measure for acute liver failure?
Increased prothrombin time
44
What are the poor prognosis indicators of liver failure?
\>Bilirubin Severe hyponatraemia Rising lactate Acidosis Rapid drop in transaminases Renal failure
45
What is the triad for acute liver failure?
Encephalopathy Jaundice Coagulopathy
46
What are the causes of hepatitis?
Autoimmune Alcohol Viral
47
What is the most common cause of hepatocellular carcinoma?
Hepatitis B most common cause worldwide and C most common in Europe
48
What do investigations show in alcoholic liver disease/alcoholic hepatitis
FBC * Macrocytic anaemia LFTs * Increased GGT * AST\>ALT in a 2:1 ratio * Low albumin
49
How is alcoholic hepatitis managed?
Glucocorticoid for acute management Vitamin K Abstinence from alcohol Nutrition support, fluids and thiamine Liver transplant Alcoholism * Chlordiazepoxide * Disulfiram * Acamprosate
50
What do investigations show in autoimmune hepatitis?
LFTs * ALT\>AST * Low albumin
51
Give features of type 1 autoimmune hepatitis
Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA) Affects both adults and children
52
Give features of type 2 autoimmune hepatitis
Anti-liver/kidney microsomal type 1 antibodies (LKM1) Affects children only
53
Give features of type 3 autoimmune hepatitis
Soluble liver-kidney antigen Affects adults in middle-age
54
What is Budd-Chiari Syndrome?
Hepatic venous outflow obstruction, leading to increased hepatic sinusoidal pressure and portal hypertension
55
What causes Budd Chiari Syndrome?
Antiphospholipid syndrome Pregnancy COCP Thrombophilia Tumour Polycythaemia rubra vera
56
How does Budd-Chiari Syndrome present?
Triad of * Sudden onset severe abdominal pain * Ascites/abdominal distention * Tender hepatomegaly
57
What investigations are used in Budd-Chiari Syndrome diagnosis?
LFTs * \>ALT/AST * ALP/Bilirubin USS with Doppler studies of the hepatic vein CT/MRI
58
How is Budd-Chiari managed?
Anticoagulation Ascites control Thrombolysis Angioplasty Transjugular Intrahepatic Portosystemic Shunt (TIPS) Liver transplant
59
What causes hepatocellular carcinoma?
Alcohol Smoking Drugs FH Associated conditions
60
What age group does hepatocellular carcinoma occur in?
Affects all age groups
61
How does hepatocellular carcinoma present?
Features of liver cirrhosis * Jaundice * Ascites * RUQ pain * Hepatomegaly * Splenomegaly * Pruritis Weight loss Cachexia
62
What conditions are associated with hepatocellular carcinoma?
Chronic hepatitis Cirrhosis Haemochromatosis Alpha1-Antitrypsin Deficiency Primary biliary cholangitis
63
What investigations are used in hepatocellualr carcinoma diagnosis?
\>Transaminases \>Alpha-fetoprotein US CT/MRI Biopsy
64
When is biopsy used in hepatocellular carcinoma?
Only if diagnosis is in question as the procedure may cause tumour spread
65
What is Hereditary Haemochromatosis (HHC)?
Autosomal recessive mutation in the HFE gene on chromosome 6, leading to abnormal iron accumulation within tissues
66
What conditions are associated with hereditary haemochromatosis?
**Think of iron deposits in other organs** Cardiomyopathy DM1 Hypothyroidism Hepatocellular carcinoma Liver cirrhosis Hypogonadism
67
How does hereditary haemochromatosis present?
Usually presents in older adults once iron overload becomes symptomatic Grey/brown pigmentation Arthalgia/joint pain, particuarly in MCP joints Fatigue Erectile dysfunction Amenorrhoea Hair loss Chronic liver disease signs * Ascites * Hepatomegaly
68
What investigations are used in hereditary haemochromatosis diagnosis?
Increased transferrin saturation * Most useful marker in general population Increased ferritin * Acute phase reactant. so can be increased with other pathology Low total iron binding capacity HFE genetic testing, diagnostic test Liver biopsy with Perls stain IgG
69
How is hereditary haemochromatosis managed?
Venesection * First line * Weekly Desferrioxamine * Medication that binds aluminium and iron
70
What is Wilson's disease?
Autosomal recessive condition characterised by abnormal hepatobiliary copper excretion, leading to neurological and hepatic symptoms
71
How does Wilson's disease present?
Speech, behaviour and psychiatric issues Kayser-Fleischer green-brown rings in iris Blue nails
72
What investigations are used in Wilson's disease diagnosis?
Decreased serum free copper Increased urinary copper Decreased caeruloplasmin USS Liver biopsy Penicillamine test
73
How is Wilson's disease managed?
D-Penicillamine * Binds to copper so it can be excreted Low copper diet Liver transplant
74
What organisms are associated with liver abscesses?
E coli in adults Staph aureus in children
75
How are liver abscesses managed?
Drainage, typically percutaneous Antibiotics * Amoxicillin + ciprofloxacin + metronidazole * If penicillin allergic ciprofloxacin + clindamycin
76
What is Gilbert's syndrome?
Benign autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase, causing a rise in bilirubin
77
How is Gilbert's syndrome managed?
Reassurance as no treatment is required

Gastrointestinal (14 decks)

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