Liver Pathology Flashcards

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
Q

How can the causes of ascites be grouped?

A

Those with a serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/L (indicating portal hypotension)

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26
Q

What are the causes of SAAG >11g/l?

A

Cirrhosis

Acute liver failure

Liver metastases

RHF

Constrictive pericarditis

Budd-Chiari syndrome

Portal vein thrombosis

Myxoedema

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27
Q

What are the causes of SAAG <11g/l?

A

Nephrotic syndrome

Malignancy

Bowel obstruction

Post-operative lymphatic leak

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28
Q

How is ascites managed?

A

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

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29
Q

What are complications of ascites?

A

Spontaneous bacterial peritonitis

Compression of IVC

Hepatorenal syndrome

Transudate pleural effusion

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30
Q

How does spontaneous bacterial peritonitis present?

A

Should always be considered in patients with known cirrhosis and ascites

Fever

Abdominal tenderness/pain

Abdominal distention

Vomiting

Altered mental state

Inflammatory markers

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31
Q

What organism typically causes spontaneous bacterial peritonitis?

A

E-coli, most commonly

Klebsiella

Staph aureus

32
Q

How is spontaneous bacterial peritonitis managed?

A

Ascitic culture prior to giving antibiotics

IV Cefotaxime

33
Q

Describe the pathophysiology of varices

A

Portal hypotension leads to the formation of collateral circulations, occurring when portal pressure exceeds 12mmHg

34
Q

What is the management of variceal haemorrhage?

A

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
Q

What is a Transjugular Intrahepatic Portosystemic Shunt (TIPS)?

A

Connection made between portal vein and hepatic vein

36
Q

What is Hepatorenal syndrome?

A

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
Q

What is the difference between type 1 and 2 hepatorenal syndrome?

A

Type 1 occurs rapidly whereas type 2 is slow progression

38
Q

What is liver failure?

A

Acute necrotizing hepatitis leading to cell destruction

39
Q

What are the 3 liver failure classifications?

A

Hyperacute or fulminant liver failure

Acute liver failure

Subacute liver failure

40
Q

What is hyperacute liver failure?

A

Encephalopathy develops within 1 week

41
Q

What is acute liver failure?

A

Encephalopathy develops within 2-4 weeks

42
Q

What is subacute liver failure?

A

Encephalopathy develops within 4-8 weeks

43
Q

What is the best measure for acute liver failure?

A

Increased prothrombin time

44
Q

What are the poor prognosis indicators of liver failure?

A

>Bilirubin

Severe hyponatraemia

Rising lactate

Acidosis

Rapid drop in transaminases

Renal failure

45
Q

What is the triad for acute liver failure?

A

Encephalopathy

Jaundice

Coagulopathy

46
Q

What are the causes of hepatitis?

A

Autoimmune

Alcohol

Viral

47
Q

What is the most common cause of hepatocellular carcinoma?

A

Hepatitis B most common cause worldwide and C most common in Europe

48
Q

What do investigations show in alcoholic liver disease/alcoholic hepatitis

A

FBC

  • Macrocytic anaemia

LFTs

  • Increased GGT
  • AST>ALT in a 2:1 ratio
  • Low albumin
49
Q

How is alcoholic hepatitis managed?

A

Glucocorticoid for acute management

Vitamin K

Abstinence from alcohol

Nutrition support, fluids and thiamine

Liver transplant

Alcoholism

  • Chlordiazepoxide
  • Disulfiram
  • Acamprosate
50
Q

What do investigations show in autoimmune hepatitis?

A

LFTs

  • ALT>AST
  • Low albumin
51
Q

Give features of type 1 autoimmune hepatitis

A

Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)

Affects both adults and children

52
Q

Give features of type 2 autoimmune hepatitis

A

Anti-liver/kidney microsomal type 1 antibodies (LKM1)

Affects children only

53
Q

Give features of type 3 autoimmune hepatitis

A

Soluble liver-kidney antigen

Affects adults in middle-age

54
Q

What is Budd-Chiari Syndrome?

A

Hepatic venous outflow obstruction, leading to increased hepatic sinusoidal pressure and portal hypertension

55
Q

What causes Budd Chiari Syndrome?

A

Antiphospholipid syndrome

Pregnancy

COCP

Thrombophilia

Tumour

Polycythaemia rubra vera

56
Q

How does Budd-Chiari Syndrome present?

A

Triad of

  • Sudden onset severe abdominal pain
  • Ascites/abdominal distention
  • Tender hepatomegaly
57
Q

What investigations are used in Budd-Chiari Syndrome diagnosis?

A

LFTs

  • >ALT/AST
  • ALP/Bilirubin

USS with Doppler studies of the hepatic vein

CT/MRI

58
Q

How is Budd-Chiari managed?

A

Anticoagulation

Ascites control

Thrombolysis

Angioplasty

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Liver transplant

59
Q

What causes hepatocellular carcinoma?

A

Alcohol

Smoking

Drugs

FH

Associated conditions

60
Q

What age group does hepatocellular carcinoma occur in?

A

Affects all age groups

61
Q

How does hepatocellular carcinoma present?

A

Features of liver cirrhosis

  • Jaundice
  • Ascites
  • RUQ pain
  • Hepatomegaly
  • Splenomegaly
  • Pruritis

Weight loss

Cachexia

62
Q

What conditions are associated with hepatocellular carcinoma?

A

Chronic hepatitis

Cirrhosis

Haemochromatosis

Alpha1-Antitrypsin Deficiency

Primary biliary cholangitis

63
Q

What investigations are used in hepatocellualr carcinoma diagnosis?

A

>Transaminases

>Alpha-fetoprotein

US

CT/MRI

Biopsy

64
Q

When is biopsy used in hepatocellular carcinoma?

A

Only if diagnosis is in question as the procedure may cause tumour spread

65
Q

What is Hereditary Haemochromatosis (HHC)?

A

Autosomal recessive mutation in the HFE gene on chromosome 6, leading to abnormal iron accumulation within tissues

66
Q

What conditions are associated with hereditary haemochromatosis?

A

Think of iron deposits in other organs

Cardiomyopathy

DM1

Hypothyroidism

Hepatocellular carcinoma

Liver cirrhosis

Hypogonadism

67
Q

How does hereditary haemochromatosis present?

A

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
Q

What investigations are used in hereditary haemochromatosis diagnosis?

A

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
Q

How is hereditary haemochromatosis managed?

A

Venesection

  • First line
  • Weekly

Desferrioxamine

  • Medication that binds aluminium and iron
70
Q

What is Wilson’s disease?

A

Autosomal recessive condition characterised by abnormal hepatobiliary copper excretion, leading to neurological and hepatic symptoms

71
Q

How does Wilson’s disease present?

A

Speech, behaviour and psychiatric issues

Kayser-Fleischer green-brown rings in iris

Blue nails

72
Q

What investigations are used in Wilson’s disease diagnosis?

A

Decreased serum free copper

Increased urinary copper

Decreased caeruloplasmin

USS

Liver biopsy

Penicillamine test

73
Q

How is Wilson’s disease managed?

A

D-Penicillamine

  • Binds to copper so it can be excreted

Low copper diet

Liver transplant

74
Q

What organisms are associated with liver abscesses?

A

E coli in adults

Staph aureus in children

75
Q

How are liver abscesses managed?

A

Drainage, typically percutaneous

Antibiotics

  • Amoxicillin + ciprofloxacin + metronidazole
  • If penicillin allergic ciprofloxacin + clindamycin
76
Q

What is Gilbert’s syndrome?

A

Benign autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase, causing a rise in bilirubin

77
Q

How is Gilbert’s syndrome managed?

A

Reassurance as no treatment is required