Cirrhosis

Question 1

Liver cirrhosis

Answer 1

Result of chronic inflammation and damage to liver cells

Cells replaced with scar tissue and nodules

Question 2

Causes

Answer 2

Alcohol

NAFLD

Viral hepatitis (B and C)

Question 3

Rarer causes

Answer 3

Autoimmune hepatitis

Primary biliary cirrhosis

Haemochromatosis

Wilsons disease

Alpha-1 antitrypsin deficiency

Cystic fibrosis

Drugs (amiodarone, methotrexate, sodium valproate)

Question 4

Signs

Answer 4

Jaundice

Hepatomegaly

Splenomegaly

Spider naevi

Palmar erythema

Gynaecomastia and testicular atrophy

Bruising

Ascites

Caput medusae

Asterixis

Question 5

Bloods

Answer 5

LFTs often normal but deranged if decompensated

Albumin decreases

Prothrombin time increases

Hyponatraemia indicates fluid retention

Urea and creatinine deranged in hepatorenal syndrome

Viral markers and autoantibodies to find cause

Alpha-fetoprotein raised in hepatocellular carcinoma

Question 6

Albumin and prothrombin time markers of

Answer 6

Synthetic function

Question 7

Enhanced liver fibrosis test

Answer 7

First line recommended investigation for NAFLD (not available in many areas)

Measures HA, PIIINP and TIMP-1

<7.7 none to mild fibrosis
>7.7-9.8 moderate fibrosis
>9.8 severe fibrosis

Question 8

Ultrasound

Answer 8

Nodularity of the surface of the liver

Corkscrew appearance of arteries with increased flow as compensating for reduced portal flow

Ascites

Splenomegaly

US patients with HCC every 6 months

Question 9

Fibroscan

Answer 9

Checks elasticity of liver by sending high frequency waves

Question 10

Endoscopy

Answer 10

To assess for and treat oesophageal varices when portal hypertension suspected

Question 11

CT and MRI scans

Answer 11

To look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessels and ascites

Question 12

Child-Pugh score

Answer 12

Indicates severity

Bilirubin

Albumin

INR

Ascites

Encephalopathy

Question 13

General management

Answer 13

US and aFP every 6 months for HCC

Endoscopy every 3 years in patients without known varices

High protein, low sodium diet

MELD score every 6 months

Consideration of liver transplant

Managing complications

Question 14

MELD score

Answer 14

Takes into account bilirubin, creatinine, INR and sodium when requiring dialysis

Gives percentage estimated 3 month mortality and helps guide referral for liver transplant

Question 15

Complications

Answer 15

Malnutrition

Portal hypertension, varices and variceal bleeding

Ascites and spontaneous bacterial peritonitis

Hepato-renal syndrome

Hepatic encephalopathy

Hepatocellular carcinoma

Question 16

Malnutrition

Answer 16

Increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth

Affects metabolism of proteins in the liver and reduces the amount of protein produced

Disrupts livers ability to store glucose as glycogen and release it when required

Results in body using muscle tissue as fuel leading to muscle wasting and weight loss

Question 17

Management of malnutrition

Answer 17

Regular meals (every 2-3 hours)

Low sodium (to minimise fluid retention)

High protein and high calorie

Avoid alcohol

Question 18

Portal vein comes from

Answer 18

Superior mesenteric vein and splenic vein

Question 19

Portal hypertension

Answer 19

Cirrhosis increases resistance of blood flow in liver

Increased back-pressure into the portal system

Causes vessels at sites where portal system anastomoses with systemic venous system to become swollen and tortuous

Question 20

Sites that varices occur

Answer 20

Gastro oesophageal junction

Ileocaecal junction

Rectum

Anterior abdominal wall via the umbilical vein (caput medusae)

Question 21

Treatment of stable varices

Answer 21

Propanolol reduces portal hypertension

Elastic band ligation

Injection of sclerosant

Transjugular intra-hepatic portosystemic shunt

Question 22

TIPS

Answer 22

Interventional radiologist inserts wire into jugular vein, down vena cava and inter liver via hepatic vein

Make connection through liver tissue between hepatic vein and portal vein and put stent in place

Allows blood to flow directly from portal vein to hepatic vein and relieves pressure in portal system and varices

Question 23

Management of bleeding oesophageal varices

Answer 23

Rescusitation
- vasopressin analogues cause vasoconstriction
- correct coagulopathy with vitamin K and fresh frozen plasma
- prophylactic broad spectrum antibiotics
- consider intubation and ICU if life threatening bleed

Urgent endoscopy
- inject sclerosant to cause inflammatory obliteration of the vessel
- elastic band ligation

Sengstaken-Blakemore tube

Question 24

Sengstaken-Blakemore tube

Answer 24

Inflatable tube inserted into oesophagus to tamponade bleeding varices

Used when endoscopy fails

Question 25

Ascites

Answer 25

Increased pressure in portal system causes fluid to leak out of capillaries in liver and bowel into peritoneal cavity Drop in circulating pressure causes reduction on BP entering kidneys Kidneys sense lower pressure and release renin, leads to increased aldosterone Cirrhosis causes transudative (low protein) content

Question 26

Spontaneous bacterial peritonitis

Answer 26

Infection developing in ascitis fluid and peritoneal lining without any clear cause

Question 27

Presentation of SBP

Answer 27

Can be asymptomatic Fever Abdominal pain Deranged bloods (raised WCC, CRP, creatinine or metabolic acidosis) Ileus Hypotension

Question 28

Most common organisms of SBP

Answer 28

Escherichia coli Klebsiella pneumoniae Gram positive cocci (staph and enterococcus)

Question 29

Management of SBP

Answer 29

Take an ascitic culture prior to giving antibiotics Usually treated with IV cephalosporin

Question 30

Hepatorenal syndrome

Answer 30

Hypertension in portal system leads to dilation of portal blood vessels Leads to loss of blood volume in kidneys Leads to hypotension in kidneys and activation of RAAS Causes renal vasoconstrction leading to starved kidneys Leads to rapid deterioration of kidney function Fatal within a week unless liver transplant performed

Question 31

Hepatic encephalopathy

Answer 31

Build up of toxin, particularly ammonia, in the brain Reduced consciousness and confusion More chronically presents with changes to personality, memory and mood

Question 32

Precipitating factors of hepatic encephalopathy

Answer 32

Constipation Electrolyte disturbance Infection GI bleed High protein diet Medications (sedatives)

Question 33

Management of hepatic encephalopathy

Answer 33

Laxatives promote excretion of ammonia Antibiotics (rifaxmin) reduces number of intestinal bacteria producing ammonia Nutritional support (may need NG tube)