6. Liver Cirrhosis Flashcards
What is cirrhosis?
Chronic inflammation damaging liver tissue, causing it to be replaced by scar tissue (fibrosis) and nodules of scar tissue form
What is portal hypertension?
Resistance to blood flow into the liver due to scar tissue formation
What are the four most common causes of liver cirrhosis?
Alcoholic liver disease
Non-alcoholic fatty liver disease
Hepatitis C
Hepatitis B
Apart from ALD, NAFLD, Hep B/C, list 7 causes of cirrhosis.
Auto-immune hepatitis
Cystic fibrosis
Primary biliary cirrhosis
Haemochromotosis
Wilson’s disease
Alpha 1 anti-trypsin deficiency
Drugs: methotrexate, sodium valproate, amioderone
2 SS specific to decompensated liver cirrhosis
Asterixis (flapping tremor) as sign of toxin build up and will cause encephalopathy
In severe cirrhosis, what do UE show?
Hyponatremia indicating sodium retention
What disease is monitored for in pts with cirrhosis and in what 2 ways, including how regularly?
HCC
Alpha-fetoprotein blood test (every 6m)
US (every 6m)
What is the ELF blood test?
Enhanced Liver Fibrosis blood test
First line investigation for assessing fibrosis in NAFLD
Measures 3 markers (HA, PIINP and TIMP-1) and uses an algorithm to generate a score
Mild/ none fibrosis: Less than 7.7
Moderate fibrosis: 7.7 to 9.8
Severe: 9.8+
How does cirrhosis present on US?
Nodularity
Corkscrew appearance of arteries
Enlarged portal vein with reduced flow
Ascites
Splenomegaly
According to NICE, who should be given a fibroscan to assess for cirrhosis every 2y?
Anyone at risk:
- Hep C (if have hep B assess yearly)
- Heavy OH drinkers (men 50+ units, women 35+ units)
- ALD
- NAFLD + evidence of fibrosis on ELF blood test
Which scoring systems are used to evaluate cirrhosis?
Childs-Pugh score: bilirubin, INR, albumin, ascites and encephalopathy are given a score or 1, 2, 3 each and score out of 15 indicates severity and prognosis
MELD score: used every 6m in patients with compensated cirrhosis, gives estimated 3m mortality and whether they need a transplant or dialysis
General management of cirrhosis
US and AFP every 6m for HCC
Endoscopy every 3y in pts w/ varices
High protein, low sodium diet
MELD score every 6m
Consider transplant
Manage complications
List the complications of cirrhosis
Malnutrition
Portal hypertension and varices
Ascites and spontaneous bacterial peritonitis
Hepato-renal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma
Why does cirrhosis cause malnutrition and how is it managed?
Cirrhosis means the liver can’t metabolise proteins and less protein is produced
Cirrhosis prevents glycogen storage and release as glucose
So muscle is used for fuel instead leading to wasting and weight loss
Managed: Regular meals (every 2-3h) Low sodium diet to limit fluid retention High protein and high calorie diet Avoid OH
The portal vein comes from which 2 veins?
Superior mesenteric and splenic
Where does PVH cause variceal formation and give 4 examples.
Where the portal system anastomoses with systemic system, varices form:
Gastro-esophageal junction
Iliocecal junction
Rectum
Anterior abdominal wall via umbilical vein (caput medusa)
How are bleeding esophageal varices treated, including the 2 aspects?
- Resuscitation
Slow bleeding with vasopressin analogues such as terlipressin
Slow bleeding with propanolol
Correct any liver disease induced coagulopathy with Vit K and FFP (contains clotting factors)
Prophylactic broad-spectrum a/b reduce mortality
Esophageal varices can exsanguanite rapidly and become life threatening so consider intubation and ICU
- Urgent endoscopy
Inject with sclerosant to cause inflammatory obliteration
Elastic band ligation of varices
If above fail, Sengstaken-Blakemore tube inserted into esophagus to tamponade bleeding varices (balloon inflated to restrict blood flow to esophagus)
Last-line: TIPS
What kind of ascites does cirrhosis cause?
Transudative (low protein)
How does cirrhosis cause ascites?
High pressure in portal system
Fluid forced out of capillaries in liver and bowel
Fluid builds up in peritoneal space
How can ascites cause AKI?
Lose circulating volume to peritoneal space
Renal hypoperfusion aka pre-renal cause of AKI
How does ascites activate the RAAS and what does this system do?
Kidneys detect low circulating volume
Release renin
Renin converts angiotensinogen to angiotensin 1
A1 gets converted into A2 by ACE in lungs
A2 causes aldosterone to be released, vasoconstriction and ADH to be released
Aldosterone causes sodium and water retention so circulating volume increases (also causes renal artery vasoconstriction to increase bp in kidneys)
Describe the management of ascites
Low sodium diet to prevent water retention
Spironolactone (potassium sparing diuretic)
Paracentesis via ascitic tap or drain
If have under 15g/L of protein in peritoneal fluid, give prophylactic a/b (ciprofloxacin or norfloxacin) for SBP
For refractory ascites consider TIPS or transplantation
What is spontaneous bacterial peritonitis?
When an infection develops in the peritoneal lining and fluid w/o any clear cause (not secondary to bowel perforation or infection due to ascitic drain)
SS of SBP
Can be asymptomatic - so have low threshold for getting ascitic fluid culture
Hypotension
Fever
Ab pain
Ileus (temporary lack of normal intestinal muscle contraction)
What blood results would indicate SBP?
Raised WCC
Raised CRP
Raised creatinine
Metabolic acidosis
Which 3 organisms most commonly cause SBP?
E.coli
Klebsiella pneumoniae
Gram positive cocci: staphylococcus or enterococcus
Prophylactic a/b given for patients with low protein ascites are ciprofloxacin or norfloxacin. How is SBP managed?
Take ascitic fluid sample for culture
IV cephalosporin such as cefotaxime
Describe hepato-renal syndrome
Fatal within a week w/o transplant
PVH leads to blood pooling in portal veins, reducing circulation elsewhere
Kidneys activate RAAS and cause renal artery vasoconstriction
Vasoconstriction + low circulating volume = kidney starved = AKI and rapidly deterorating kidney function
Describe hepatic encephalopathy aka portosystemic encephalopathy and explain the role of ammonia in it
Liver stops functioning
Toxins build up
Ammonia builds up in particular
Made in gut by intestinal breakdown on protein break-down and absorbed by gut
In cirrhosis liver can’t metabolise ammonia and collateral vessels form between portal and systemic circulation, so ammonia can bypass the liver
Management of hepatic encephalopathy
Laxatives (lactulose) to clear ammonia from gut before it enters systemic circulation. Aim for 2-3 soft motions/d. Enemas may be required initially.
A/B (rifaximin) to reduce the amount of bacteria in the gut so less ammonia produced
Nutritional support (may need nasogastric feeding)
SS of HE
Acute: reduced consciousness and confusion
Chronic: personality, memory and mood changes
Percipitating HE factors
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative)
In cirrhosis, which tests should be done?
Viral markers
Auto-antibodies
